| First Author | Galli D | Year | 2015 |
| Journal | Exp Cell Res | Volume | 330 |
| Issue | 2 | Pages | 277-86 |
| PubMed ID | 25433270 | Mgi Jnum | J:218608 |
| Mgi Id | MGI:5618040 | Doi | 10.1016/j.yexcr.2014.11.011 |
| Citation | Galli D, et al. (2015) PKCepsilon is a negative regulator of PVAT-derived vessel formation. Exp Cell Res 330(2):277-86 |
| abstractText | RATIONALE: Vessel formation is a crucial event in tissue repair after injury. Thus, one assumption of innovative therapeutic approaches is the understanding of its molecular mechanisms. Notwithstanding our knowledge of the role of Protein Kinase C epsilon (PKCepsilon) in cardio-protection and vascular restenosis, its role in vessel progenitor differentiation remains elusive. OBJECTIVE: Given the availability of PKCepsilon pharmacological modulators already tested in clinical trials, the specific aim of this study is to unravel the role of PKCepsilon in vessel progenitor differentiation, with implications in vascular pathology and vasculogenesis. METHODS AND RESULTS: Mouse Peri-Vascular Adipose Tissue (PVAT) was used as source of mesenchymal vessel progenitors. VEGF-induced differentiation of PVAT cells down-regulates both PKCepsilon and p-PAK1 protein expression levels. PKCepsilon overexpression and activation: i) reduced the expression levels of SMA and PECAM in endothelial differentiation of PVAT cells; ii) completely abrogated tubules formation in collagen gel assays; iii) increased the expression of p-PAK1. CONCLUSION: PKCepsilon negatively interferes with vessel progenitor differentiation via interaction with PAK-1. |
