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首页> 外文期刊>Cellular Signalling >Gax inhibits perivascular preadipocyte biofunction mediated by IGF-1 induced FAK/Pyk2 and ERK2 cooperative pathways
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Gax inhibits perivascular preadipocyte biofunction mediated by IGF-1 induced FAK/Pyk2 and ERK2 cooperative pathways

机译：Gax抑制由IGF-1诱导的FAK / Pyk2和ERK2协同途径介导的血管前脂肪细胞生物功能

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摘要

Perivascular adipocyte (PVAC) biofunctionswere closely related to cardiovascular diseases; its specific biological mechanisms remained unclear. Howto adjust PVAC functions of vascular cells is an important topic. The present study was designed to investigate whether FAK/Pyk2 and ERK1/2MAPK 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 adipocytewere cultured, dedifferentiated, and stimulatedwith 10nMIGF-I. Cellular function experiments showed that IGF-1 promoted PVAC proliferation, adhesion, and migration. However Gax weakened IGF- 1-mediated these function. Flowcytometry 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 interferewith these signaling pathways and inhibit PVAC functions.
机译：血管周围脂肪细胞（PVAC）的生物功能与心血管疾病密切相关;其具体的生物学机制仍不清楚。如何调节血管细胞的PVAC功能是重要的课题。本研究旨在研究FAK / Pyk2和ERK1 / 2MAPK信号通路是否参与PVAC功能，该功能由胰岛素样生长因子1（IGF-1）激活并被Gax抑制。从血管周脂肪细胞分离的PVAC用10nMIGF-I培养，去分化和刺激。细胞功能实验表明，IGF-1促进PVAC增殖，粘附和迁移。但是，Gax减弱了IGF-1介导的这些功能。流式细胞仪表明，IGF-1增加了S期的PVACs百分比，降低了G0 / G1期和凋亡细胞的百分比。 Gax降低了S期细胞的百分率，增加了G0-G1期和凋亡细胞的百分率。Westernblotting和RT-PCR显示IGF-1激活FAK / Pyk2和ERK1 / 2信号通路，上调mRNA和蛋白表达。 FAK，Pyk2和ERK1 / 2的抑制，并抑制p53表达。相反，Gax降低了这些信号蛋白的表达，并增加了p53的表达。因此，IGF-1介导的FAK / Pyk2和ERK1 / 2途径可增强PVAC功能。 Gax有效抵消了IGF-1的这些作用，抑制了PVAC活性，并增加了细胞凋亡。我们的发现表明，IGF-1介导的FAK / Pyk2和ERK1 / 2协同激活对于PVAC功能至关重要，而Gax是有希望的候选基因，可以干扰这些信号通路并抑制PVAC功能。

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