ArticlePloS one2013
PECAM1(+)/Sca1(+)/CD38(+) vascular cells transform into myofibroblast-like cells in skin wound repair.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 26 citations in OpenAlex.
- Multi-omics data reveal the origin of cardiac myxoma.Communications biology · 2025Article
- trans-Endothelial neutrophil migration activates bactericidal function via Piezo1 mechanosensing.Immunity · 2024Article
- Dysregulated CD38 expression in blood and skin immune cells of patients with hidradenitis suppurativa.Research square · 2023Article
- Monitoring Wound Healing with Topically Applied Optical NanoFlare mRNA Nanosensors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Heterogeneous subpopulations of adventitial progenitor cells regulate vascular homeostasis and pathological vascular remodelling.Cardiovascular research · 2022Review
- Gene Expression Profiling of the Extracellular Matrix Signature in Macrophages of Different Activation Status: Relevance for Skin Wound Healing.International journal of molecular sciences · 2019Article
- Interaction between a 3D collagen matrix used for periodontal soft tissue regeneration and T-lymphocytes: AnExperimental and therapeutic medicine · 2019Article
- Stromal CD38 regulates outgrowth of primary melanoma and generation of spontaneous metastasis.Oncotarget · 2018Article
- Scar-free cutaneous wound healing in the leopard gecko, Eublepharis macularius.Journal of anatomy · 2015Article
- Immunohistological localization of endogenous unlabeled stem cells in wounded skin.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2014Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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