| First Author | Zhu X | Year | 2017 |
| Journal | Biochem Biophys Res Commun | Volume | 484 |
| Issue | 1 | Pages | 144-151 |
| PubMed ID | 28093232 | Mgi Jnum | J:250876 |
| Mgi Id | MGI:6101589 | Doi | 10.1016/j.bbrc.2017.01.054 |
| Citation | Zhu X, et al. (2017) Phospholipase Cepsilon deficiency delays the early stage of cutaneous wound healing and attenuates scar formation in mice. Biochem Biophys Res Commun 484(1):144-151 |
| abstractText | This study aimed to investigate the role of phospholipase Cepsilon (PLCepsilon) in the skin wound healing process. PLCepsilon, an effect factor of Ras/Rap small G protein, plays a crucial role in skin inflammation by regulating inflammatory cytokines. Inflammatory responses are closely associated with wound healing. Full-thickness skin wounds were made in the PLCepsilon knockout (KO) and wild-type (WT) mice, and the healing process was analyzed. The macroscopic wound closure rate declined in the PLCepsilon KO mice on days 3, 4, and 5 after wounding, following the decreased expression of interleukin (IL)-6, chemokine (C-X-C motif) ligand (Cxcl)-1, Cxcl-2, and chemokine (C-C motif) ligand (Ccl) 20. The proliferation rate of epidermal keratinocytes was not affected by PLCepsilon, but silencing of PLCepsilon resulted in the delayed migration of keratinocytes. Moreover, the scars were found to be much smaller in the PLCepsilon KO mice than in the WT mice. The mRNA expression of Ccl20, collagen (Col) 6a1, and Col17a1 decreased in the PLCepsilon KO mice. These results were in agreement with a previous hypothesis that PLCepsilon might delay the early stage of cutaneous wound healing by inhibiting the migration of keratinocytes, and decrease the expression of Col6a1, Col17a1, and Ccl20 by inhibiting the inflammatory response to reduce scar formation. This study shed light on a novel role of PLCepsilon in wound healing and provided new therapeutic approaches to target PLCepsilon for diminishing scar formation after injury. |
