PKCδ Regulates Force Signaling during VEGF/CXCL4 Induced Dissociation of Endothelial Tubes
Identifieur interne : 001947 ( Ncbi/Curation ); précédent : 001946; suivant : 001948PKCδ Regulates Force Signaling during VEGF/CXCL4 Induced Dissociation of Endothelial Tubes
Auteurs : Joshua Jamison [États-Unis] ; James H-C. Wang [États-Unis] ; Alan Wells [États-Unis]Source :
- PLoS ONE [ 1932-6203 ] ; 2014.
Descripteurs français
- KwdFr :
- Cellules cultivées, Cellules endothéliales (), Cellules endothéliales (métabolisme), Cicatrisation de plaie (), Cicatrisation de plaie (physiologie), Endothélium vasculaire (), Endothélium vasculaire (métabolisme), Facteur de croissance endothéliale vasculaire de type A (pharmacologie), Facteur-4 plaquettaire (pharmacologie), Humains, Indoles (pharmacologie), Mouvement cellulaire (), Mouvement cellulaire (physiologie), Néovascularisation physiologique (), Néovascularisation physiologique (physiologie), Protein kinase C-delta (métabolisme), Pyrroles (pharmacologie).
- MESH :
- métabolisme : Cellules endothéliales, Endothélium vasculaire, Protein kinase C-delta.
- pharmacologie : Facteur de croissance endothéliale vasculaire de type A, Facteur-4 plaquettaire, Indoles, Pyrroles.
- physiologie : Cicatrisation de plaie, Mouvement cellulaire, Néovascularisation physiologique.
- Cellules cultivées, Cellules endothéliales, Cicatrisation de plaie, Endothélium vasculaire, Humains, Mouvement cellulaire, Néovascularisation physiologique.
English descriptors
- KwdEn :
- Cell Movement (drug effects), Cell Movement (physiology), Cells, Cultured, Endothelial Cells (drug effects), Endothelial Cells (metabolism), Endothelium, Vascular (drug effects), Endothelium, Vascular (metabolism), Humans, Indoles (pharmacology), Neovascularization, Physiologic (drug effects), Neovascularization, Physiologic (physiology), Platelet Factor 4 (pharmacology), Protein Kinase C-delta (metabolism), Pyrroles (pharmacology), Vascular Endothelial Growth Factor A (pharmacology), Wound Healing (drug effects), Wound Healing (physiology).
- MESH :
- chemical , metabolism : Protein Kinase C-delta.
- chemical , pharmacology : Indoles, Platelet Factor 4, Pyrroles, Vascular Endothelial Growth Factor A.
- drug effects : Cell Movement, Endothelial Cells, Endothelium, Vascular, Neovascularization, Physiologic, Wound Healing.
- metabolism : Endothelial Cells, Endothelium, Vascular.
- physiology : Cell Movement, Neovascularization, Physiologic, Wound Healing.
- Cells, Cultured, Humans.
Abstract
Wound healing requires the vasculature to re-establish itself from the severed ends; endothelial cells within capillaries must detach from neighboring cells before they can migrate into the nascent wound bed to initiate angiogenesis. The dissociation of these endothelial capillaries is driven partially by platelets' release of growth factors and cytokines, particularly the chemokine CXCL4/platelet factor-4 (PF4) that increases cell-cell de-adherence. As this retraction is partly mediated by increased transcellular contractility, the protein kinase c-δ/myosin light chain-2 (PKCδ/MLC-2) signaling axis becomes a candidate mechanism to drive endothelial dissociation. We hypothesize that PKCδ activation induces contractility through MLC-2 to promote dissociation of endothelial cords after exposure to platelet-released CXCL4 and VEGF. To investigate this mechanism of contractility, endothelial cells were allowed to form cords following CXCL4 addition to perpetuate cord dissociation. In this study, CXCL4-induced dissociation was reduced by a VEGFR inhibitor (sunitinib malate) and/or PKCδ inhibition. During combined CXCL4+VEGF treatment, increased contractility mediated by MLC-2 that is dependent on PKCδ regulation. As cellular force is transmitted to focal adhesions, zyxin, a focal adhesion protein that is mechano-responsive, was upregulated after PKCδ inhibition. This study suggests that growth factor regulation of PKCδ may be involved in CXCL4-mediated dissociation of endothelial cords.
Url:
DOI: 10.1371/journal.pone.0093968
PubMed: 24699667
PubMed Central: 3974837
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PMC:3974837Le document en format XML
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Wang</name><affiliation wicri:level="4"><nlm:aff id="aff2"><addr-line>Department of Orthopedic Surgery, McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Orthopedic Surgery, McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania</wicri:regionArea><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation></author><author><name sortKey="Wells, Alan" sort="Wells, Alan" uniqKey="Wells A" first="Alan" last="Wells">Alan Wells</name><affiliation wicri:level="4"><nlm:aff id="aff1"><addr-line>Department of Pathology, McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania</wicri:regionArea><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Movement (drug effects)</term><term>Cell Movement (physiology)</term><term>Cells, Cultured</term><term>Endothelial Cells (drug effects)</term><term>Endothelial Cells (metabolism)</term><term>Endothelium, Vascular (drug effects)</term><term>Endothelium, Vascular (metabolism)</term><term>Humans</term><term>Indoles (pharmacology)</term><term>Neovascularization, Physiologic (drug effects)</term><term>Neovascularization, Physiologic (physiology)</term><term>Platelet Factor 4 (pharmacology)</term><term>Protein Kinase C-delta (metabolism)</term><term>Pyrroles (pharmacology)</term><term>Vascular Endothelial Growth Factor A (pharmacology)</term><term>Wound Healing (drug effects)</term><term>Wound Healing (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Cellules cultivées</term><term>Cellules endothéliales ()</term><term>Cellules endothéliales (métabolisme)</term><term>Cicatrisation de plaie ()</term><term>Cicatrisation de plaie (physiologie)</term><term>Endothélium vasculaire ()</term><term>Endothélium vasculaire (métabolisme)</term><term>Facteur de croissance endothéliale vasculaire de type A (pharmacologie)</term><term>Facteur-4 plaquettaire (pharmacologie)</term><term>Humains</term><term>Indoles (pharmacologie)</term><term>Mouvement cellulaire ()</term><term>Mouvement cellulaire (physiologie)</term><term>Néovascularisation physiologique ()</term><term>Néovascularisation physiologique (physiologie)</term><term>Protein kinase C-delta (métabolisme)</term><term>Pyrroles (pharmacologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Protein Kinase C-delta</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Indoles</term><term>Platelet Factor 4</term><term>Pyrroles</term><term>Vascular Endothelial Growth Factor A</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Movement</term><term>Endothelial Cells</term><term>Endothelium, Vascular</term><term>Neovascularization, Physiologic</term><term>Wound Healing</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelial Cells</term><term>Endothelium, Vascular</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules endothéliales</term><term>Endothélium vasculaire</term><term>Protein kinase C-delta</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type A</term><term>Facteur-4 plaquettaire</term><term>Indoles</term><term>Pyrroles</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Cicatrisation de plaie</term><term>Mouvement cellulaire</term><term>Néovascularisation physiologique</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Movement</term><term>Neovascularization, Physiologic</term><term>Wound Healing</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cells, Cultured</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules cultivées</term><term>Cellules endothéliales</term><term>Cicatrisation de plaie</term><term>Endothélium vasculaire</term><term>Humains</term><term>Mouvement cellulaire</term><term>Néovascularisation physiologique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Wound healing requires the vasculature to re-establish itself from the severed ends; endothelial cells within capillaries must detach from neighboring cells before they can migrate into the nascent wound bed to initiate angiogenesis. The dissociation of these endothelial capillaries is driven partially by platelets' release of growth factors and cytokines, particularly the chemokine CXCL4/platelet factor-4 (PF4) that increases cell-cell de-adherence. As this retraction is partly mediated by increased transcellular contractility, the protein kinase c-δ/myosin light chain-2 (PKCδ/MLC-2) signaling axis becomes a candidate mechanism to drive endothelial dissociation. We hypothesize that PKCδ activation induces contractility through MLC-2 to promote dissociation of endothelial cords after exposure to platelet-released CXCL4 and VEGF. To investigate this mechanism of contractility, endothelial cells were allowed to form cords following CXCL4 addition to perpetuate cord dissociation. In this study, CXCL4-induced dissociation was reduced by a VEGFR inhibitor (sunitinib malate) and/or PKCδ inhibition. During combined CXCL4+VEGF treatment, increased contractility mediated by MLC-2 that is dependent on PKCδ regulation. As cellular force is transmitted to focal adhesions, zyxin, a focal adhesion protein that is mechano-responsive, was upregulated after PKCδ inhibition. This study suggests that growth factor regulation of PKCδ may be involved in CXCL4-mediated dissociation of endothelial cords.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Li, J" uniqKey="Li J">J Li</name></author><author><name sortKey="Zhang, Yp" uniqKey="Zhang Y">YP Zhang</name></author><author><name sortKey="Kirsner, Rs" uniqKey="Kirsner R">RS Kirsner</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chen, P" uniqKey="Chen P">P Chen</name></author><author><name sortKey="Gupta, K" uniqKey="Gupta K">K Gupta</name></author><author><name sortKey="Wells, A" uniqKey="Wells A">A Wells</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chen, P" uniqKey="Chen P">P Chen</name></author><author><name sortKey="Xie, H" uniqKey="Xie H">H Xie</name></author><author><name sortKey="Sekar, Mc" uniqKey="Sekar M">MC Sekar</name></author><author><name sortKey="Gupta, K" uniqKey="Gupta K">K Gupta</name></author><author><name sortKey="Wells, A" uniqKey="Wells A">A Wells</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shizukuda, Y" uniqKey="Shizukuda Y">Y Shizukuda</name></author><author><name sortKey="Tang, S" uniqKey="Tang S">S Tang</name></author><author><name sortKey="Yokota, R" uniqKey="Yokota R">R Yokota</name></author><author><name sortKey="Ware, Ja" uniqKey="Ware J">JA Ware</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yamamura, S" uniqKey="Yamamura S">S Yamamura</name></author><author><name sortKey="Nelson, Pr" uniqKey="Nelson P">PR Nelson</name></author><author><name sortKey="Kent, Kc" uniqKey="Kent K">KC Kent</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Joyce, Nc" uniqKey="Joyce N">NC Joyce</name></author><author><name sortKey="Meklir, B" uniqKey="Meklir B">B Meklir</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jamison, J" uniqKey="Jamison J">J Jamison</name></author><author><name sortKey="Lauffenburger, D" uniqKey="Lauffenburger D">D Lauffenburger</name></author><author><name sortKey="Wang, Jc" uniqKey="Wang J">JC Wang</name></author><author><name sortKey="Wells, A" uniqKey="Wells A">A Wells</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Iwabu, A" uniqKey="Iwabu A">A Iwabu</name></author><author><name sortKey="Smith, K" uniqKey="Smith K">K Smith</name></author><author><name sortKey="Allen, Fd" uniqKey="Allen F">FD Allen</name></author><author><name sortKey="Lauffenburger, Da" uniqKey="Lauffenburger D">DA Lauffenburger</name></author><author><name sortKey="Wells, A" uniqKey="Wells A">A Wells</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wells, A" uniqKey="Wells A">A Wells</name></author><author><name sortKey="Ware, Mf" uniqKey="Ware M">MF Ware</name></author><author><name sortKey="Allen, Fd" uniqKey="Allen F">FD Allen</name></author><author><name sortKey="Lauffenburger, Da" uniqKey="Lauffenburger D">DA Lauffenburger</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Insall, Rh" uniqKey="Insall R">RH Insall</name></author><author><name sortKey="Weiner, Od" uniqKey="Weiner O">OD Weiner</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shao, H" uniqKey="Shao H">H Shao</name></author><author><name sortKey="Chou, J" uniqKey="Chou J">J Chou</name></author><author><name sortKey="Baty, Cj" uniqKey="Baty C">CJ Baty</name></author><author><name sortKey="Burke, Na" uniqKey="Burke N">NA Burke</name></author><author><name sortKey="Watkins, Sc" uniqKey="Watkins S">SC Watkins</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ron, D" uniqKey="Ron D">D Ron</name></author><author><name sortKey="Kazanietz, Mg" uniqKey="Kazanietz M">MG Kazanietz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Stahelin, Rv" uniqKey="Stahelin R">RV Stahelin</name></author><author><name sortKey="Digman, Ma" uniqKey="Digman M">MA Digman</name></author><author><name sortKey="Medkova, M" uniqKey="Medkova M">M Medkova</name></author><author><name sortKey="Ananthanarayanan, B" uniqKey="Ananthanarayanan B">B Ananthanarayanan</name></author><author><name sortKey="Melowic, Hr" uniqKey="Melowic H">HR Melowic</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Seki, T" uniqKey="Seki T">T Seki</name></author><author><name sortKey="Matsubayashi, H" uniqKey="Matsubayashi H">H Matsubayashi</name></author><author><name sortKey="Amano, T" uniqKey="Amano T">T Amano</name></author><author><name sortKey="Shirai, Y" uniqKey="Shirai Y">Y Shirai</name></author><author><name sortKey="Saito, N" uniqKey="Saito N">N 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sortKey="Swerlick, Ra" uniqKey="Swerlick R">RA Swerlick</name></author><author><name sortKey="George, Vg" uniqKey="George V">VG George</name></author><author><name sortKey="Summers, S" uniqKey="Summers S">S Summers</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, Q" uniqKey="Li Q">Q Li</name></author><author><name sortKey="Subbulakshmi, V" uniqKey="Subbulakshmi V">V Subbulakshmi</name></author><author><name sortKey="Fields, Ap" uniqKey="Fields A">AP Fields</name></author><author><name sortKey="Murray, Nr" uniqKey="Murray N">NR Murray</name></author><author><name sortKey="Cathcart, Mk" uniqKey="Cathcart M">MK Cathcart</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Woo, Ch" uniqKey="Woo C">CH Woo</name></author><author><name sortKey="Lim, Jh" uniqKey="Lim J">JH Lim</name></author><author><name sortKey="Kim, Jh" uniqKey="Kim J">JH 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