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Gax inhibits perivascular preadipocyte biofunction mediated by IGF-1 induced FAK/Pyk2 and ERK2 cooperative pathways.

Abstract：

:Perivascular adipocyte (PVAC) biofunctions were closely related to cardiovascular diseases; its specific biological mechanisms remained unclear. How to adjust PVAC functions of vascular cells is an important topic. The present study was designed to investigate whether FAK/Pyk2 and ERK1/2 MAPK signaling pathways participate in PVAC functions, which is activated by insulin-like growth factor 1(IGF-1) and inhibited by Gax. PVACs isolated from perivascular adipocyte were cultured, dedifferentiated, and stimulated with 10nM IGF-I. Cellular function experiments showed that IGF-1 promoted PVAC proliferation, adhesion, and migration. However Gax weakened IGF-1-mediated these function. Flow cytometry demonstrated that IGF-1 increased PVACs percent of S phase and decreased the percent of G0/G1 phase and apoptotic cells. While, Gax decreased the percent of S phase cells and increased those of G0-G1 phase and apoptotic cells. Western blotting and RT-PCR revealed that IGF-1 activated FAK/Pyk2 and ERK1/2 signaling pathways, upregulated the mRNA and protein expression of FAK, Pyk2, and ERK1/2, and suppressed p53 expression. Reversely, Gax lowered the expression of these signaling proteins and increased p53 expression. Therefore, IGF-1 mediated FAK/Pyk2 and ERK1/2 pathways to augment PVAC functions; Gax effectively counteracted these effects of IGF-1, repressed PVAC activities, and increased the cell apoptosis. Our findings suggested that FAK/Pyk2 and ERK1/2 cooperative activation mediated by IGF-1 is essential for PVAC functions, and Gax is a promising candidate gene to interfere with these signaling pathways and inhibit PVAC functions.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Liu P,Feng J,Kong F,Lu Q,Xu H,Meng J,Jiang Y

doi

10.1016/j.cellsig.2014.09.017

subject

Has Abstract

pub_date

2014-12-01 00:00:00

pages

3036-45

issue

12

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(14)00321-0

journal_volume

26

pub_type

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