Glutaredoxin-1 up-regulation induces soluble vascular endothelial growth factor receptor 1, attenuating post-ischemia limb revascularization.
Identifieur interne : 000652 ( Main/Exploration ); précédent : 000651; suivant : 000653Glutaredoxin-1 up-regulation induces soluble vascular endothelial growth factor receptor 1, attenuating post-ischemia limb revascularization.
Auteurs : Colin E. Murdoch ; Michaela Shuler ; Dagmar J F. Haeussler ; Ryosuke Kikuchi ; Priyanka Bearelly ; Jingyan Han ; Yosuke Watanabe ; José J. Fuster ; Kenneth Walsh ; Ye-Shih Ho ; Markus M. Bachschmid ; Richard A. Cohen ; Reiko MatsuiSource :
- The Journal of biological chemistry [ 1083-351X ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Cellules cultivées (MeSH), Cellules endothéliales (métabolisme), Facteur de transcription NF-kappa B (métabolisme), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Humains (MeSH), Ischémie (génétique), Ischémie (métabolisme), Ischémie (physiopathologie), Membre pelvien (physiopathologie), Membre pelvien (vascularisation), Mouvement cellulaire (MeSH), Néovascularisation physiologique (MeSH), Protéine Wnt-5a (MeSH), Protéines de type Wingless (métabolisme), Protéines proto-oncogènes (métabolisme), Récepteur-1 au facteur croissance endothéliale vasculaire (métabolisme), Régulation positive (MeSH), Souris (MeSH), Souris transgéniques (MeSH).
- MESH :
- génétique : Glutarédoxines, Ischémie.
- métabolisme : Cellules endothéliales, Facteur de transcription NF-kappa B, Glutarédoxines, Ischémie, Protéines de type Wingless, Protéines proto-oncogènes, Récepteur-1 au facteur croissance endothéliale vasculaire.
- physiopathologie : Ischémie, Membre pelvien.
- vascularisation : Membre pelvien.
- Animaux, Cellules cultivées, Humains, Mouvement cellulaire, Néovascularisation physiologique, Protéine Wnt-5a, Régulation positive, Souris, Souris transgéniques.
English descriptors
- KwdEn :
- Animals (MeSH), Cell Movement (MeSH), Cells, Cultured (MeSH), Endothelial Cells (metabolism), Glutaredoxins (genetics), Glutaredoxins (metabolism), Hindlimb (blood supply), Hindlimb (physiopathology), Humans (MeSH), Ischemia (genetics), Ischemia (metabolism), Ischemia (physiopathology), Mice (MeSH), Mice, Transgenic (MeSH), NF-kappa B (metabolism), Neovascularization, Physiologic (MeSH), Proto-Oncogene Proteins (metabolism), Up-Regulation (MeSH), Vascular Endothelial Growth Factor Receptor-1 (metabolism), Wnt Proteins (metabolism), Wnt-5a Protein (MeSH).
- MESH :
- chemical , genetics : Glutaredoxins.
- blood supply : Hindlimb.
- genetics : Ischemia.
- metabolism : Endothelial Cells, Glutaredoxins, Ischemia, NF-kappa B, Proto-Oncogene Proteins, Vascular Endothelial Growth Factor Receptor-1, Wnt Proteins.
- physiopathology : Hindlimb, Ischemia.
- Animals, Cell Movement, Cells, Cultured, Humans, Mice, Mice, Transgenic, Neovascularization, Physiologic, Up-Regulation, Wnt-5a Protein.
Abstract
Glutaredoxin-1 (Glrx) is a cytosolic enzyme that regulates diverse cellular function by removal of GSH adducts from S-glutathionylated proteins including signaling molecules and transcription factors. Glrx is up-regulated during inflammation and diabetes, and Glrx overexpression inhibits VEGF-induced EC migration. The aim was to investigate the role of up-regulated Glrx in EC angiogenic capacities and in vivo revascularization in the setting of hind limb ischemia. Glrx-overexpressing EC from Glrx transgenic (TG) mice showed impaired migration and network formation and secreted higher levels of soluble VEGF receptor 1 (sFlt), an antagonizing factor to VEGF. After hind limb ischemia surgery Glrx TG mice demonstrated impaired blood flow recovery, associated with lower capillary density and poorer limb motor function compared with wild type littermates. There were also higher levels of anti-angiogenic sFlt expression in the muscle and plasma of Glrx TG mice after surgery. Noncanonical Wnt5a is known to induce sFlt. Wnt5a was highly expressed in ischemic muscles and EC from Glrx TG mice, and exogenous Wnt5a induced sFlt expression and inhibited network formation in human microvascular EC. Adenoviral Glrx-induced sFlt in EC was inhibited by a competitive Wnt5a inhibitor. Furthermore, Glrx overexpression removed GSH adducts on p65 in ischemic muscle and EC and enhanced NF-κB activity, which was responsible for Wnt5a-sFlt induction. Taken together, up-regulated Glrx induces sFlt in EC via NF-κB-dependent Wnt5a, resulting in attenuated revascularization in hind limb ischemia. The Glrx-induced sFlt explains part of the mechanism of redox-regulated VEGF signaling.
DOI: 10.1074/jbc.M113.517219
PubMed: 24482236
PubMed Central: PMC3961686
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Murdoch</name><affiliation><nlm:affiliation>From the Vascular Biology Section and.</nlm:affiliation><wicri:noCountry code="no comma">From the Vascular Biology Section and.</wicri:noCountry></affiliation></author><author><name sortKey="Shuler, Michaela" sort="Shuler, Michaela" uniqKey="Shuler M" first="Michaela" last="Shuler">Michaela Shuler</name></author><author><name sortKey="Haeussler, Dagmar J F" sort="Haeussler, Dagmar J F" uniqKey="Haeussler D" first="Dagmar J F" last="Haeussler">Dagmar J F. Haeussler</name></author><author><name sortKey="Kikuchi, Ryosuke" sort="Kikuchi, Ryosuke" uniqKey="Kikuchi R" first="Ryosuke" last="Kikuchi">Ryosuke Kikuchi</name></author><author><name sortKey="Bearelly, Priyanka" sort="Bearelly, Priyanka" uniqKey="Bearelly P" first="Priyanka" last="Bearelly">Priyanka Bearelly</name></author><author><name sortKey="Han, Jingyan" sort="Han, Jingyan" uniqKey="Han J" first="Jingyan" last="Han">Jingyan Han</name></author><author><name sortKey="Watanabe, Yosuke" sort="Watanabe, Yosuke" uniqKey="Watanabe Y" first="Yosuke" last="Watanabe">Yosuke Watanabe</name></author><author><name sortKey="Fuster, Jose J" sort="Fuster, Jose J" uniqKey="Fuster J" first="José J" last="Fuster">José J. Fuster</name></author><author><name sortKey="Walsh, Kenneth" sort="Walsh, Kenneth" uniqKey="Walsh K" first="Kenneth" last="Walsh">Kenneth Walsh</name></author><author><name sortKey="Ho, Ye Shih" sort="Ho, Ye Shih" uniqKey="Ho Y" first="Ye-Shih" last="Ho">Ye-Shih Ho</name></author><author><name sortKey="Bachschmid, Markus M" sort="Bachschmid, Markus M" uniqKey="Bachschmid M" first="Markus M" last="Bachschmid">Markus M. Bachschmid</name></author><author><name sortKey="Cohen, Richard A" sort="Cohen, Richard A" uniqKey="Cohen R" first="Richard A" last="Cohen">Richard A. Cohen</name></author><author><name sortKey="Matsui, Reiko" sort="Matsui, Reiko" uniqKey="Matsui R" first="Reiko" last="Matsui">Reiko Matsui</name></author></analytic><series><title level="j">The Journal of biological chemistry</title><idno type="eISSN">1083-351X</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Cell Movement (MeSH)</term><term>Cells, Cultured (MeSH)</term><term>Endothelial Cells (metabolism)</term><term>Glutaredoxins (genetics)</term><term>Glutaredoxins (metabolism)</term><term>Hindlimb (blood supply)</term><term>Hindlimb (physiopathology)</term><term>Humans (MeSH)</term><term>Ischemia (genetics)</term><term>Ischemia (metabolism)</term><term>Ischemia (physiopathology)</term><term>Mice (MeSH)</term><term>Mice, Transgenic (MeSH)</term><term>NF-kappa B (metabolism)</term><term>Neovascularization, Physiologic (MeSH)</term><term>Proto-Oncogene Proteins (metabolism)</term><term>Up-Regulation (MeSH)</term><term>Vascular Endothelial Growth Factor Receptor-1 (metabolism)</term><term>Wnt Proteins (metabolism)</term><term>Wnt-5a Protein (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Cellules cultivées (MeSH)</term><term>Cellules endothéliales (métabolisme)</term><term>Facteur de transcription NF-kappa B (métabolisme)</term><term>Glutarédoxines (génétique)</term><term>Glutarédoxines (métabolisme)</term><term>Humains (MeSH)</term><term>Ischémie (génétique)</term><term>Ischémie (métabolisme)</term><term>Ischémie (physiopathologie)</term><term>Membre pelvien (physiopathologie)</term><term>Membre pelvien (vascularisation)</term><term>Mouvement cellulaire (MeSH)</term><term>Néovascularisation physiologique (MeSH)</term><term>Protéine Wnt-5a (MeSH)</term><term>Protéines de type Wingless (métabolisme)</term><term>Protéines proto-oncogènes (métabolisme)</term><term>Récepteur-1 au facteur croissance endothéliale vasculaire (métabolisme)</term><term>Régulation positive (MeSH)</term><term>Souris (MeSH)</term><term>Souris transgéniques (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="genetics" xml:lang="en"><term>Ischemia</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glutarédoxines</term><term>Ischémie</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelial Cells</term><term>Glutaredoxins</term><term>Ischemia</term><term>NF-kappa B</term><term>Proto-Oncogene Proteins</term><term>Vascular Endothelial Growth Factor Receptor-1</term><term>Wnt Proteins</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules endothéliales</term><term>Facteur de transcription NF-kappa B</term><term>Glutarédoxines</term><term>Ischémie</term><term>Protéines de type Wingless</term><term>Protéines proto-oncogènes</term><term>Récepteur-1 au facteur croissance endothéliale vasculaire</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Ischémie</term><term>Membre pelvien</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Hindlimb</term><term>Ischemia</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>Cell Movement</term><term>Cells, Cultured</term><term>Humans</term><term>Mice</term><term>Mice, Transgenic</term><term>Neovascularization, Physiologic</term><term>Up-Regulation</term><term>Wnt-5a Protein</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Humains</term><term>Mouvement cellulaire</term><term>Néovascularisation physiologique</term><term>Protéine Wnt-5a</term><term>Régulation positive</term><term>Souris</term><term>Souris transgéniques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Glutaredoxin-1 (Glrx) is a cytosolic enzyme that regulates diverse cellular function by removal of GSH adducts from S-glutathionylated proteins including signaling molecules and transcription factors. Glrx is up-regulated during inflammation and diabetes, and Glrx overexpression inhibits VEGF-induced EC migration. The aim was to investigate the role of up-regulated Glrx in EC angiogenic capacities and in vivo revascularization in the setting of hind limb ischemia. Glrx-overexpressing EC from Glrx transgenic (TG) mice showed impaired migration and network formation and secreted higher levels of soluble VEGF receptor 1 (sFlt), an antagonizing factor to VEGF. After hind limb ischemia surgery Glrx TG mice demonstrated impaired blood flow recovery, associated with lower capillary density and poorer limb motor function compared with wild type littermates. There were also higher levels of anti-angiogenic sFlt expression in the muscle and plasma of Glrx TG mice after surgery. Noncanonical Wnt5a is known to induce sFlt. Wnt5a was highly expressed in ischemic muscles and EC from Glrx TG mice, and exogenous Wnt5a induced sFlt expression and inhibited network formation in human microvascular EC. Adenoviral Glrx-induced sFlt in EC was inhibited by a competitive Wnt5a inhibitor. Furthermore, Glrx overexpression removed GSH adducts on p65 in ischemic muscle and EC and enhanced NF-κB activity, which was responsible for Wnt5a-sFlt induction. Taken together, up-regulated Glrx induces sFlt in EC via NF-κB-dependent Wnt5a, resulting in attenuated revascularization in hind limb ischemia. The Glrx-induced sFlt explains part of the mechanism of redox-regulated VEGF signaling.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24482236</PMID><DateCompleted><Year>2014</Year><Month>05</Month><Day>27</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1083-351X</ISSN><JournalIssue CitedMedium="Internet"><Volume>289</Volume><Issue>12</Issue><PubDate><Year>2014</Year><Month>Mar</Month><Day>21</Day></PubDate></JournalIssue><Title>The Journal of biological chemistry</Title><ISOAbbreviation>J Biol Chem</ISOAbbreviation></Journal><ArticleTitle>Glutaredoxin-1 up-regulation induces soluble vascular endothelial growth factor receptor 1, attenuating post-ischemia limb revascularization.</ArticleTitle><Pagination><MedlinePgn>8633-44</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1074/jbc.M113.517219</ELocationID><Abstract><AbstractText>Glutaredoxin-1 (Glrx) is a cytosolic enzyme that regulates diverse cellular function by removal of GSH adducts from S-glutathionylated proteins including signaling molecules and transcription factors. Glrx is up-regulated during inflammation and diabetes, and Glrx overexpression inhibits VEGF-induced EC migration. The aim was to investigate the role of up-regulated Glrx in EC angiogenic capacities and in vivo revascularization in the setting of hind limb ischemia. Glrx-overexpressing EC from Glrx transgenic (TG) mice showed impaired migration and network formation and secreted higher levels of soluble VEGF receptor 1 (sFlt), an antagonizing factor to VEGF. After hind limb ischemia surgery Glrx TG mice demonstrated impaired blood flow recovery, associated with lower capillary density and poorer limb motor function compared with wild type littermates. There were also higher levels of anti-angiogenic sFlt expression in the muscle and plasma of Glrx TG mice after surgery. Noncanonical Wnt5a is known to induce sFlt. Wnt5a was highly expressed in ischemic muscles and EC from Glrx TG mice, and exogenous Wnt5a induced sFlt expression and inhibited network formation in human microvascular EC. Adenoviral Glrx-induced sFlt in EC was inhibited by a competitive Wnt5a inhibitor. Furthermore, Glrx overexpression removed GSH adducts on p65 in ischemic muscle and EC and enhanced NF-κB activity, which was responsible for Wnt5a-sFlt induction. Taken together, up-regulated Glrx induces sFlt in EC via NF-κB-dependent Wnt5a, resulting in attenuated revascularization in hind limb ischemia. The Glrx-induced sFlt explains part of the mechanism of redox-regulated VEGF signaling.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Murdoch</LastName><ForeName>Colin E</ForeName><Initials>CE</Initials><AffiliationInfo><Affiliation>From the Vascular Biology Section and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shuler</LastName><ForeName>Michaela</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Haeussler</LastName><ForeName>Dagmar J F</ForeName><Initials>DJ</Initials></Author><Author ValidYN="Y"><LastName>Kikuchi</LastName><ForeName>Ryosuke</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Bearelly</LastName><ForeName>Priyanka</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Han</LastName><ForeName>Jingyan</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Watanabe</LastName><ForeName>Yosuke</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Fuster</LastName><ForeName>José J</ForeName><Initials>JJ</Initials></Author><Author ValidYN="Y"><LastName>Walsh</LastName><ForeName>Kenneth</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Ho</LastName><ForeName>Ye-Shih</ForeName><Initials>YS</Initials></Author><Author ValidYN="Y"><LastName>Bachschmid</LastName><ForeName>Markus M</ForeName><Initials>MM</Initials></Author><Author ValidYN="Y"><LastName>Cohen</LastName><ForeName>Richard A</ForeName><Initials>RA</Initials></Author><Author ValidYN="Y"><LastName>Matsui</LastName><ForeName>Reiko</ForeName><Initials>R</Initials></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>HL081587</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL007224</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 HL081587</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 HL068758</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 HL 068758</GrantID><Acronym>HL</Acronym><Agency>NHLBI 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>2014</Year><Month>01</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Biol Chem</MedlineTA><NlmUniqueID>2985121R</NlmUniqueID><ISSNLinking>0021-9258</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011518">Proto-Oncogene Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C085389">WNT5A protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051153">Wnt Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000071818">Wnt-5a Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="C501162">FLT1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="C501163">Flt1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D040281">Vascular Endothelial Growth Factor Receptor-1</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002465" MajorTopicYN="N">Cell Movement</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006614" MajorTopicYN="N">Hindlimb</DescriptorName><QualifierName UI="Q000098" MajorTopicYN="Y">blood supply</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007511" MajorTopicYN="N">Ischemia</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018919" MajorTopicYN="N">Neovascularization, Physiologic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011518" MajorTopicYN="N">Proto-Oncogene Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D040281" MajorTopicYN="N">Vascular Endothelial Growth Factor Receptor-1</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051153" MajorTopicYN="N">Wnt Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000071818" MajorTopicYN="N">Wnt-5a Protein</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Angiogenesis</Keyword><Keyword MajorTopicYN="N">Animal Models</Keyword><Keyword MajorTopicYN="N">Glutathionylation</Keyword><Keyword MajorTopicYN="N">Ischemia</Keyword><Keyword MajorTopicYN="N">NF-kappa B (NF-κB)</Keyword><Keyword MajorTopicYN="N">Redox Regulation</Keyword><Keyword MajorTopicYN="N">Vascular Endothelial Growth Factor (VEGF)</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>2</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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