PECAM1(+)/Sca1(+)/CD38(+) vascular cells transform into myofibroblast-like cells in skin wound repair.
Skin injury induces the formation of new blood vessels by activating the vasculature in order to restore tissue homeostasis. Vascular cells may also differentiate into matrix-secreting contractile myofibroblasts to promote wound closure. Here, we characterize a PECAM1(+)/Sca1(+) vascular cell popula...
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Format: | Article |
Language: | English |
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Public Library of Science (PLoS)
2013-01-01
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Series: | PLoS ONE |
Online Access: | http://europepmc.org/articles/PMC3537615?pdf=render |
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author | Julia Etich Vera Bergmeier Christian Frie Sandra Kreft Lena Bengestrate Sabine Eming Cornelia Mauch Beate Eckes Hikmet Ulus Frances E Lund Gunter Rappl Hinrich Abken Mats Paulsson Bent Brachvogel |
author_facet | Julia Etich Vera Bergmeier Christian Frie Sandra Kreft Lena Bengestrate Sabine Eming Cornelia Mauch Beate Eckes Hikmet Ulus Frances E Lund Gunter Rappl Hinrich Abken Mats Paulsson Bent Brachvogel |
author_sort | Julia Etich |
collection | DOAJ |
description | Skin injury induces the formation of new blood vessels by activating the vasculature in order to restore tissue homeostasis. Vascular cells may also differentiate into matrix-secreting contractile myofibroblasts to promote wound closure. Here, we characterize a PECAM1(+)/Sca1(+) vascular cell population in mouse skin, which is highly enriched in wounds at the peak of neoangiogenesis and myofibroblast formation. These cells express endothelial and perivascular markers and present the receptor CD38 on their surface. PECAM1(+)/Sca1(+)/CD38(+) cells proliferate upon wounding and could give rise to α-SMA(+) myofibroblast-like cells. CD38 stimulation in immunodeficient mice reduced the wound size at the peak of neoangiogenesis and myofibroblast formation. In humans a corresponding cell population was identified, which was enriched in sprouting vessels of basal cell carcinoma biopsies. The results indicate that PECAM1(+)/Sca1(+)/CD38(+) vascular cells could proliferate and differentiate into myofibroblast-like cells in wound repair. Moreover, CD38 signaling modulates PECAM1(+)/Sca1(+)/CD38(+) cell activation in the healing process implying CD38 as a target for anti-angiogenic therapies in human basal cell carcinoma. |
first_indexed | 2024-12-13T07:47:01Z |
format | Article |
id | doaj.art-c701b6905739460c9a7918665f80248f |
institution | Directory Open Access Journal |
issn | 1932-6203 |
language | English |
last_indexed | 2024-12-13T07:47:01Z |
publishDate | 2013-01-01 |
publisher | Public Library of Science (PLoS) |
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series | PLoS ONE |
spelling | doaj.art-c701b6905739460c9a7918665f80248f2022-12-21T23:54:48ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0181e5326210.1371/journal.pone.0053262PECAM1(+)/Sca1(+)/CD38(+) vascular cells transform into myofibroblast-like cells in skin wound repair.Julia EtichVera BergmeierChristian FrieSandra KreftLena BengestrateSabine EmingCornelia MauchBeate EckesHikmet UlusFrances E LundGunter RapplHinrich AbkenMats PaulssonBent BrachvogelSkin injury induces the formation of new blood vessels by activating the vasculature in order to restore tissue homeostasis. Vascular cells may also differentiate into matrix-secreting contractile myofibroblasts to promote wound closure. Here, we characterize a PECAM1(+)/Sca1(+) vascular cell population in mouse skin, which is highly enriched in wounds at the peak of neoangiogenesis and myofibroblast formation. These cells express endothelial and perivascular markers and present the receptor CD38 on their surface. PECAM1(+)/Sca1(+)/CD38(+) cells proliferate upon wounding and could give rise to α-SMA(+) myofibroblast-like cells. CD38 stimulation in immunodeficient mice reduced the wound size at the peak of neoangiogenesis and myofibroblast formation. In humans a corresponding cell population was identified, which was enriched in sprouting vessels of basal cell carcinoma biopsies. The results indicate that PECAM1(+)/Sca1(+)/CD38(+) vascular cells could proliferate and differentiate into myofibroblast-like cells in wound repair. Moreover, CD38 signaling modulates PECAM1(+)/Sca1(+)/CD38(+) cell activation in the healing process implying CD38 as a target for anti-angiogenic therapies in human basal cell carcinoma.http://europepmc.org/articles/PMC3537615?pdf=render |
spellingShingle | Julia Etich Vera Bergmeier Christian Frie Sandra Kreft Lena Bengestrate Sabine Eming Cornelia Mauch Beate Eckes Hikmet Ulus Frances E Lund Gunter Rappl Hinrich Abken Mats Paulsson Bent Brachvogel PECAM1(+)/Sca1(+)/CD38(+) vascular cells transform into myofibroblast-like cells in skin wound repair. PLoS ONE |
title | PECAM1(+)/Sca1(+)/CD38(+) vascular cells transform into myofibroblast-like cells in skin wound repair. |
title_full | PECAM1(+)/Sca1(+)/CD38(+) vascular cells transform into myofibroblast-like cells in skin wound repair. |
title_fullStr | PECAM1(+)/Sca1(+)/CD38(+) vascular cells transform into myofibroblast-like cells in skin wound repair. |
title_full_unstemmed | PECAM1(+)/Sca1(+)/CD38(+) vascular cells transform into myofibroblast-like cells in skin wound repair. |
title_short | PECAM1(+)/Sca1(+)/CD38(+) vascular cells transform into myofibroblast-like cells in skin wound repair. |
title_sort | pecam1 sca1 cd38 vascular cells transform into myofibroblast like cells in skin wound repair |
url | http://europepmc.org/articles/PMC3537615?pdf=render |
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