PKCε is a negative regulator of PVAT-derived vessel formation.

Abstract:

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 (PKCε) in cardio-protection and vascular restenosis, its role in vessel progenitor differentiation remains elusive. OBJECTIVE:Given the availability of PKCε pharmacological modulators already tested in clinical trials, the specific aim of this study is to unravel the role of PKCε 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 PKCε and p-PAK1 protein expression levels. PKCε 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:PKCε negatively interferes with vessel progenitor differentiation via interaction with PAK-1.

journal_name

Exp Cell Res

authors

Galli D,Carubbi C,Masselli E,Corradi D,Dei Cas A,Nouvenne A,Bucci G,Arcari ML,Mirandola P,Vitale M,Gobbi G

doi

10.1016/j.yexcr.2014.11.011

subject

Has Abstract

pub_date

2015-01-15 00:00:00

pages

277-286

issue

2

eissn

0014-4827

issn

1090-2422

pii

S0014-4827(14)00507-2

journal_volume

330

pub_type

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