PKCε is a negative regulator of PVAT-derived vessel formation.
Exp Cell Res
; 330(2): 277-286, 2015 Jan 15.
Article
em En
| MEDLINE
| ID: mdl-25433270
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 ANDRESULTS:
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.Palavras-chave
Texto completo:
1
Bases de dados:
MEDLINE
Assunto principal:
Tecido Adiposo
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Neovascularização Fisiológica
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Células Endoteliais
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Proteína Quinase C-épsilon
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Quinases Ativadas por p21
Limite:
Animals
Idioma:
En
Revista:
Exp Cell Res
Ano de publicação:
2015
Tipo de documento:
Article
País de afiliação:
Itália