Endothelial cell-specific redox gene modulation inhibits angiogenesis but promotes B16F0 tumor growth in mice.
Identifieur interne : 000173 ( Main/Exploration ); précédent : 000172; suivant : 000174Endothelial cell-specific redox gene modulation inhibits angiogenesis but promotes B16F0 tumor growth in mice.
Auteurs : Yoshimitsu Yura [États-Unis] ; Brian S H. Chong [États-Unis] ; Ryan D. Johnson [États-Unis] ; Yosuke Watanabe [États-Unis] ; Yuko Tsukahara [États-Unis] ; Beatriz Ferran [États-Unis] ; Colin E. Murdoch [États-Unis] ; Jessica B. Behring [États-Unis] ; Mark E. Mccomb [États-Unis] ; Catherine E. Costello [États-Unis] ; Yvonne M W. Janssen-Heininger [États-Unis] ; Richard A. Cohen [États-Unis] ; Markus M. Bachschmid [États-Unis] ; Reiko Matsui [États-Unis]Source :
- FASEB journal : official publication of the Federation of American Societies for Experimental Biology [ 1530-6860 ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Artère fémorale (chirurgie), Cellules endothéliales (métabolisme), Femelle (MeSH), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Ischémie (MeSH), Ligature (MeSH), Membre pelvien (chirurgie), Membre pelvien (vascularisation), Mâle (MeSH), Mélanome (traitement médicamenteux), Néovascularisation pathologique (métabolisme), Néovascularisation physiologique (effets des médicaments et des substances chimiques), Souris (MeSH), Souris transgéniques (MeSH), Tumeurs expérimentales (MeSH).
- MESH :
- chirurgie : Artère fémorale, Membre pelvien.
- effets des médicaments et des substances chimiques : Néovascularisation physiologique.
- génétique : Glutarédoxines.
- métabolisme : Cellules endothéliales, Glutarédoxines, Néovascularisation pathologique.
- traitement médicamenteux : Mélanome.
- vascularisation : Membre pelvien.
- Animaux, Femelle, Ischémie, Ligature, Mâle, Souris, Souris transgéniques, Tumeurs expérimentales.
English descriptors
- KwdEn :
- Animals (MeSH), Endothelial Cells (metabolism), Female (MeSH), Femoral Artery (surgery), Glutaredoxins (genetics), Glutaredoxins (metabolism), Hindlimb (blood supply), Hindlimb (surgery), Ischemia (MeSH), Ligation (MeSH), Male (MeSH), Melanoma (drug therapy), Mice (MeSH), Mice, Transgenic (MeSH), Neoplasms, Experimental (MeSH), Neovascularization, Pathologic (metabolism), Neovascularization, Physiologic (drug effects).
- MESH :
- chemical , genetics : Glutaredoxins.
- blood supply : Hindlimb.
- drug effects : Neovascularization, Physiologic.
- drug therapy : Melanoma.
- metabolism : Endothelial Cells, Glutaredoxins, Neovascularization, Pathologic.
- surgery : Femoral Artery, Hindlimb.
- Animals, Female, Ischemia, Ligation, Male, Mice, Mice, Transgenic, Neoplasms, Experimental.
Abstract
Glutaredoxin-1 (Glrx) is a small cytosolic enzyme that removes S-glutathionylation, glutathione adducts of protein cysteine residues, thus modulating redox signaling and gene transcription. Although Glrx up-regulation prevented endothelial cell (EC) migration and global Glrx transgenic mice had impaired ischemic vascularization, the effects of cell-specific Glrx overexpression remained unknown. Here, we examined the role of EC-specific Glrx up-regulation in distinct models of angiogenesis; namely, hind limb ischemia and tumor angiogenesis. EC-specific Glrx transgenic (EC-Glrx TG) overexpression in mice significantly impaired EC migration in Matrigel implants and hind limb revascularization after femoral artery ligation. Additionally, ECs migrated less into subcutaneously implanted B16F0 melanoma tumors as assessed by decreased staining of EC markers. Despite reduced angiogenesis, EC-Glrx TG mice unexpectedly developed larger tumors compared with control mice. EC-Glrx TG mice showed higher levels of VEGF-A in the tumors, indicating hypoxia, which may stimulate tumor cells to form vascular channels without EC, referred to as vasculogenic mimicry. These data suggest that impaired ischemic vascularization does not necessarily associate with suppression of tumor growth, and that antiangiogenic therapies may be ineffective for melanoma tumors because of their ability to implement vasculogenic mimicry during hypoxia.-Yura, Y., Chong, B. S. H., Johnson, R. D., Watanabe, Y., Tsukahara, Y., Ferran, B., Murdoch, C. E., Behring, J. B., McComb, M. E., Costello, C. E., Janssen-Heininger, Y. M. W., Cohen, R. A., Bachschmid, M. M., Matsui, R. Endothelial cell-specific redox gene modulation inhibits angiogenesis but promotes B16F0 tumor growth in mice.
DOI: 10.1096/fj.201900786R
PubMed: 31647879
PubMed Central: PMC6894059
Affiliations:
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Johnson</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Watanabe, Yosuke" sort="Watanabe, Yosuke" uniqKey="Watanabe Y" first="Yosuke" last="Watanabe">Yosuke Watanabe</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Tsukahara, Yuko" sort="Tsukahara, Yuko" uniqKey="Tsukahara Y" first="Yuko" last="Tsukahara">Yuko Tsukahara</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Ferran, Beatriz" sort="Ferran, Beatriz" uniqKey="Ferran B" first="Beatriz" last="Ferran">Beatriz Ferran</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Murdoch, Colin E" sort="Murdoch, Colin E" uniqKey="Murdoch C" first="Colin E" last="Murdoch">Colin E. Murdoch</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Behring, Jessica B" sort="Behring, Jessica B" uniqKey="Behring J" first="Jessica B" last="Behring">Jessica B. Behring</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Mccomb, Mark E" sort="Mccomb, Mark E" uniqKey="Mccomb M" first="Mark E" last="Mccomb">Mark E. Mccomb</name><affiliation wicri:level="2"><nlm:affiliation>Cardiovascular Proteomics Center, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Cardiovascular Proteomics Center, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Costello, Catherine E" sort="Costello, Catherine E" uniqKey="Costello C" first="Catherine E" last="Costello">Catherine E. Costello</name><affiliation wicri:level="2"><nlm:affiliation>Cardiovascular Proteomics Center, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Cardiovascular Proteomics Center, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Janssen Heininger, Yvonne M W" sort="Janssen Heininger, Yvonne M W" uniqKey="Janssen Heininger Y" first="Yvonne M W" last="Janssen-Heininger">Yvonne M W. Janssen-Heininger</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pathology and Laboratory Medicine, University of Vermont, Burlington, Vermont, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Laboratory Medicine, University of Vermont, Burlington, Vermont</wicri:regionArea><placeName><region type="state">Vermont</region></placeName></affiliation></author><author><name sortKey="Cohen, Richard A" sort="Cohen, Richard A" uniqKey="Cohen R" first="Richard A" last="Cohen">Richard A. Cohen</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Bachschmid, Markus M" sort="Bachschmid, Markus M" uniqKey="Bachschmid M" first="Markus M" last="Bachschmid">Markus M. Bachschmid</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Matsui, Reiko" sort="Matsui, Reiko" uniqKey="Matsui R" first="Reiko" last="Matsui">Reiko Matsui</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:31647879</idno><idno type="pmid">31647879</idno><idno type="doi">10.1096/fj.201900786R</idno><idno type="pmc">PMC6894059</idno><idno type="wicri:Area/Main/Corpus">000102</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000102</idno><idno type="wicri:Area/Main/Curation">000102</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000102</idno><idno type="wicri:Area/Main/Exploration">000102</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Endothelial cell-specific redox gene modulation inhibits angiogenesis but promotes B16F0 tumor growth in mice.</title><author><name sortKey="Yura, Yoshimitsu" sort="Yura, Yoshimitsu" uniqKey="Yura Y" first="Yoshimitsu" last="Yura">Yoshimitsu Yura</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Chong, Brian S H" sort="Chong, Brian S H" uniqKey="Chong B" first="Brian S H" last="Chong">Brian S H. Chong</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Johnson, Ryan D" sort="Johnson, Ryan D" uniqKey="Johnson R" first="Ryan D" last="Johnson">Ryan D. Johnson</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Watanabe, Yosuke" sort="Watanabe, Yosuke" uniqKey="Watanabe Y" first="Yosuke" last="Watanabe">Yosuke Watanabe</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Tsukahara, Yuko" sort="Tsukahara, Yuko" uniqKey="Tsukahara Y" first="Yuko" last="Tsukahara">Yuko Tsukahara</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Ferran, Beatriz" sort="Ferran, Beatriz" uniqKey="Ferran B" first="Beatriz" last="Ferran">Beatriz Ferran</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Murdoch, Colin E" sort="Murdoch, Colin E" uniqKey="Murdoch C" first="Colin E" last="Murdoch">Colin E. Murdoch</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Behring, Jessica B" sort="Behring, Jessica B" uniqKey="Behring J" first="Jessica B" last="Behring">Jessica B. Behring</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Mccomb, Mark E" sort="Mccomb, Mark E" uniqKey="Mccomb M" first="Mark E" last="Mccomb">Mark E. Mccomb</name><affiliation wicri:level="2"><nlm:affiliation>Cardiovascular Proteomics Center, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Cardiovascular Proteomics Center, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Costello, Catherine E" sort="Costello, Catherine E" uniqKey="Costello C" first="Catherine E" last="Costello">Catherine E. Costello</name><affiliation wicri:level="2"><nlm:affiliation>Cardiovascular Proteomics Center, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Cardiovascular Proteomics Center, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Janssen Heininger, Yvonne M W" sort="Janssen Heininger, Yvonne M W" uniqKey="Janssen Heininger Y" first="Yvonne M W" last="Janssen-Heininger">Yvonne M W. Janssen-Heininger</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pathology and Laboratory Medicine, University of Vermont, Burlington, Vermont, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Laboratory Medicine, University of Vermont, Burlington, Vermont</wicri:regionArea><placeName><region type="state">Vermont</region></placeName></affiliation></author><author><name sortKey="Cohen, Richard A" sort="Cohen, Richard A" uniqKey="Cohen R" first="Richard A" last="Cohen">Richard A. Cohen</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Bachschmid, Markus M" sort="Bachschmid, Markus M" uniqKey="Bachschmid M" first="Markus M" last="Bachschmid">Markus M. Bachschmid</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Matsui, Reiko" sort="Matsui, Reiko" uniqKey="Matsui R" first="Reiko" last="Matsui">Reiko Matsui</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author></analytic><series><title level="j">FASEB journal : official publication of the Federation of American Societies for Experimental Biology</title><idno type="eISSN">1530-6860</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Endothelial Cells (metabolism)</term><term>Female (MeSH)</term><term>Femoral Artery (surgery)</term><term>Glutaredoxins (genetics)</term><term>Glutaredoxins (metabolism)</term><term>Hindlimb (blood supply)</term><term>Hindlimb (surgery)</term><term>Ischemia (MeSH)</term><term>Ligation (MeSH)</term><term>Male (MeSH)</term><term>Melanoma (drug therapy)</term><term>Mice (MeSH)</term><term>Mice, Transgenic (MeSH)</term><term>Neoplasms, Experimental (MeSH)</term><term>Neovascularization, Pathologic (metabolism)</term><term>Neovascularization, Physiologic (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Artère fémorale (chirurgie)</term><term>Cellules endothéliales (métabolisme)</term><term>Femelle (MeSH)</term><term>Glutarédoxines (génétique)</term><term>Glutarédoxines (métabolisme)</term><term>Ischémie (MeSH)</term><term>Ligature (MeSH)</term><term>Membre pelvien (chirurgie)</term><term>Membre pelvien (vascularisation)</term><term>Mâle (MeSH)</term><term>Mélanome (traitement médicamenteux)</term><term>Néovascularisation pathologique (métabolisme)</term><term>Néovascularisation physiologique (effets des médicaments et des substances chimiques)</term><term>Souris (MeSH)</term><term>Souris transgéniques (MeSH)</term><term>Tumeurs expérimentales (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Hindlimb</term></keywords><keywords scheme="MESH" qualifier="chirurgie" xml:lang="fr"><term>Artère fémorale</term><term>Membre pelvien</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Neovascularization, Physiologic</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Melanoma</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Néovascularisation physiologique</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glutarédoxines</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelial Cells</term><term>Glutaredoxins</term><term>Neovascularization, Pathologic</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules endothéliales</term><term>Glutarédoxines</term><term>Néovascularisation pathologique</term></keywords><keywords scheme="MESH" qualifier="surgery" xml:lang="en"><term>Femoral Artery</term><term>Hindlimb</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Mélanome</term></keywords><keywords scheme="MESH" qualifier="vascularisation" xml:lang="fr"><term>Membre pelvien</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Ischemia</term><term>Ligation</term><term>Male</term><term>Mice</term><term>Mice, Transgenic</term><term>Neoplasms, Experimental</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Ischémie</term><term>Ligature</term><term>Mâle</term><term>Souris</term><term>Souris transgéniques</term><term>Tumeurs expérimentales</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Glutaredoxin-1 (Glrx) is a small cytosolic enzyme that removes <i>S</i>-glutathionylation, glutathione adducts of protein cysteine residues, thus modulating redox signaling and gene transcription. Although Glrx up-regulation prevented endothelial cell (EC) migration and global Glrx transgenic mice had impaired ischemic vascularization, the effects of cell-specific Glrx overexpression remained unknown. Here, we examined the role of EC-specific Glrx up-regulation in distinct models of angiogenesis; namely, hind limb ischemia and tumor angiogenesis. EC-specific Glrx transgenic (EC-Glrx TG) overexpression in mice significantly impaired EC migration in Matrigel implants and hind limb revascularization after femoral artery ligation. Additionally, ECs migrated less into subcutaneously implanted B16F0 melanoma tumors as assessed by decreased staining of EC markers. Despite reduced angiogenesis, EC-Glrx TG mice unexpectedly developed larger tumors compared with control mice. EC-Glrx TG mice showed higher levels of VEGF-A in the tumors, indicating hypoxia, which may stimulate tumor cells to form vascular channels without EC, referred to as vasculogenic mimicry. These data suggest that impaired ischemic vascularization does not necessarily associate with suppression of tumor growth, and that antiangiogenic therapies may be ineffective for melanoma tumors because of their ability to implement vasculogenic mimicry during hypoxia.-Yura, Y., Chong, B. S. H., Johnson, R. D., Watanabe, Y., Tsukahara, Y., Ferran, B., Murdoch, C. E., Behring, J. B., McComb, M. E., Costello, C. E., Janssen-Heininger, Y. M. W., Cohen, R. A., Bachschmid, M. M., Matsui, R. Endothelial cell-specific redox gene modulation inhibits angiogenesis but promotes B16F0 tumor growth in mice.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31647879</PMID><DateCompleted><Year>2020</Year><Month>06</Month><Day>26</Day></DateCompleted><DateRevised><Year>2020</Year><Month>11</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1530-6860</ISSN><JournalIssue CitedMedium="Internet"><Volume>33</Volume><Issue>12</Issue><PubDate><Year>2019</Year><Month>12</Month></PubDate></JournalIssue><Title>FASEB journal : official publication of the Federation of American Societies for Experimental Biology</Title><ISOAbbreviation>FASEB J</ISOAbbreviation></Journal><ArticleTitle>Endothelial cell-specific redox gene modulation inhibits angiogenesis but promotes B16F0 tumor growth in mice.</ArticleTitle><Pagination><MedlinePgn>14147-14158</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1096/fj.201900786R</ELocationID><Abstract><AbstractText>Glutaredoxin-1 (Glrx) is a small cytosolic enzyme that removes <i>S</i>-glutathionylation, glutathione adducts of protein cysteine residues, thus modulating redox signaling and gene transcription. Although Glrx up-regulation prevented endothelial cell (EC) migration and global Glrx transgenic mice had impaired ischemic vascularization, the effects of cell-specific Glrx overexpression remained unknown. Here, we examined the role of EC-specific Glrx up-regulation in distinct models of angiogenesis; namely, hind limb ischemia and tumor angiogenesis. EC-specific Glrx transgenic (EC-Glrx TG) overexpression in mice significantly impaired EC migration in Matrigel implants and hind limb revascularization after femoral artery ligation. Additionally, ECs migrated less into subcutaneously implanted B16F0 melanoma tumors as assessed by decreased staining of EC markers. Despite reduced angiogenesis, EC-Glrx TG mice unexpectedly developed larger tumors compared with control mice. EC-Glrx TG mice showed higher levels of VEGF-A in the tumors, indicating hypoxia, which may stimulate tumor cells to form vascular channels without EC, referred to as vasculogenic mimicry. These data suggest that impaired ischemic vascularization does not necessarily associate with suppression of tumor growth, and that antiangiogenic therapies may be ineffective for melanoma tumors because of their ability to implement vasculogenic mimicry during hypoxia.-Yura, Y., Chong, B. S. H., Johnson, R. D., Watanabe, Y., Tsukahara, Y., Ferran, B., Murdoch, C. E., Behring, J. B., McComb, M. E., Costello, C. E., Janssen-Heininger, Y. M. W., Cohen, R. A., Bachschmid, M. M., Matsui, R. Endothelial cell-specific redox gene modulation inhibits angiogenesis but promotes B16F0 tumor growth in mice.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Yura</LastName><ForeName>Yoshimitsu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Chong</LastName><ForeName>Brian S H</ForeName><Initials>BSH</Initials><AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Johnson</LastName><ForeName>Ryan D</ForeName><Initials>RD</Initials><AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Watanabe</LastName><ForeName>Yosuke</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tsukahara</LastName><ForeName>Yuko</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ferran</LastName><ForeName>Beatriz</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Murdoch</LastName><ForeName>Colin E</ForeName><Initials>CE</Initials><AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Behring</LastName><ForeName>Jessica B</ForeName><Initials>JB</Initials><AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McComb</LastName><ForeName>Mark E</ForeName><Initials>ME</Initials><AffiliationInfo><Affiliation>Cardiovascular Proteomics Center, Boston University School of Medicine, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Costello</LastName><ForeName>Catherine E</ForeName><Initials>CE</Initials><AffiliationInfo><Affiliation>Cardiovascular Proteomics Center, Boston University School of Medicine, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Janssen-Heininger</LastName><ForeName>Yvonne M W</ForeName><Initials>YMW</Initials><AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, University of Vermont, Burlington, Vermont, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cohen</LastName><ForeName>Richard A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bachschmid</LastName><ForeName>Markus M</ForeName><Initials>MM</Initials><AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Matsui</LastName><ForeName>Reiko</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HHSN268201000031C</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 HL007224</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R35 HL135828</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL137268</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL133013</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R03 AG051857</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>UL1 TR001430</GrantID><Acronym>TR</Acronym><Agency>NCATS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DK103750</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R37 HL104017</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>10</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>FASEB J</MedlineTA><NlmUniqueID>8804484</NlmUniqueID><ISSNLinking>0892-6638</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C516006">Glrx protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005263" MajorTopicYN="N">Femoral Artery</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006614" MajorTopicYN="N">Hindlimb</DescriptorName><QualifierName UI="Q000098" MajorTopicYN="N">blood supply</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007511" MajorTopicYN="N">Ischemia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008026" MajorTopicYN="N">Ligation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008545" MajorTopicYN="N">Melanoma</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009374" MajorTopicYN="N">Neoplasms, Experimental</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009389" MajorTopicYN="N">Neovascularization, Pathologic</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018919" MajorTopicYN="N">Neovascularization, Physiologic</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">S-glutathionylation</Keyword><Keyword MajorTopicYN="Y">glutaredoxin</Keyword><Keyword MajorTopicYN="Y">melanoma</Keyword><Keyword MajorTopicYN="Y">vascular</Keyword><Keyword MajorTopicYN="Y">vasculogenic mimicry</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>10</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>6</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>10</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31647879</ArticleId><ArticleId IdType="doi">10.1096/fj.201900786R</ArticleId><ArticleId 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Bachschmid</name><name sortKey="Behring, Jessica B" sort="Behring, Jessica B" uniqKey="Behring J" first="Jessica B" last="Behring">Jessica B. Behring</name><name sortKey="Chong, Brian S H" sort="Chong, Brian S H" uniqKey="Chong B" first="Brian S H" last="Chong">Brian S H. Chong</name><name sortKey="Cohen, Richard A" sort="Cohen, Richard A" uniqKey="Cohen R" first="Richard A" last="Cohen">Richard A. Cohen</name><name sortKey="Costello, Catherine E" sort="Costello, Catherine E" uniqKey="Costello C" first="Catherine E" last="Costello">Catherine E. Costello</name><name sortKey="Ferran, Beatriz" sort="Ferran, Beatriz" uniqKey="Ferran B" first="Beatriz" last="Ferran">Beatriz Ferran</name><name sortKey="Janssen Heininger, Yvonne M W" sort="Janssen Heininger, Yvonne M W" uniqKey="Janssen Heininger Y" first="Yvonne M W" last="Janssen-Heininger">Yvonne M W. Janssen-Heininger</name><name sortKey="Johnson, Ryan D" sort="Johnson, Ryan D" uniqKey="Johnson R" first="Ryan D" last="Johnson">Ryan D. Johnson</name><name sortKey="Matsui, Reiko" sort="Matsui, Reiko" uniqKey="Matsui R" first="Reiko" last="Matsui">Reiko Matsui</name><name sortKey="Mccomb, Mark E" sort="Mccomb, Mark E" uniqKey="Mccomb M" first="Mark E" last="Mccomb">Mark E. Mccomb</name><name sortKey="Murdoch, Colin E" sort="Murdoch, Colin E" uniqKey="Murdoch C" first="Colin E" last="Murdoch">Colin E. Murdoch</name><name sortKey="Tsukahara, Yuko" sort="Tsukahara, Yuko" uniqKey="Tsukahara Y" first="Yuko" last="Tsukahara">Yuko Tsukahara</name><name sortKey="Watanabe, Yosuke" sort="Watanabe, Yosuke" uniqKey="Watanabe Y" first="Yosuke" last="Watanabe">Yosuke Watanabe</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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