Cui Liwen, Bai Yaling, Zhang Junxia, Zhang Shenglei, Xu Jinsheng
a Department of Nephrology , The Fourth Affiliated Hospital of Hebei Medical University , Shijiazhuang City , Hebei Province , China.
Clin Exp Hypertens. 2016;38(5):451-6. doi: 10.3109/10641963.2016.1163366. Epub 2016 Jun 30.
Recent studies have indicated that extracellular acid stimulation inhibited the calcification of vascular smooth muscle cells (VSMCs). Cell apoptosis played an important role in the occurrence and development of vascular calcification. We further explored the effects of Gas6/Axl or PI3K/Akt signaling pathway on the inhibition of rat VSMCs calcification in response to extracellular acid stimulation. Our study demonstrated that a high concentration of phosphorus induced apoptosis and calcification of VSMCs, decreased expression of Axl, and reduced phosphorylation of Akt. Stimulation of extracellular acid counteracted the effects as above by increasing the expression of Axl and Akt phosphorylation and decreasing the expression of activated Caspase3, which thereby decreased cell apoptosis and calcification. Moreover, the effects can be attenuated by PI3K inhibitor. Our study proved that extracellular acid stimulation played a vital role in the inhibition of rat VSMCs calcification and apoptosis in Gas6/Axl or PI3K/Akt signaling pathway.
最近的研究表明，细胞外酸性刺激可抑制血管平滑肌细胞（VSMC）的钙化。细胞凋亡在血管钙化的发生和发展中起重要作用。我们进一步探讨了Gas6/Axl或PI3K/Akt信号通路对细胞外酸性刺激下大鼠VSMC钙化抑制的影响。我们的研究表明，高浓度磷可诱导VSMC凋亡和钙化，降低Axl表达，并减少Akt磷酸化。细胞外酸性刺激通过增加Axl表达和Akt磷酸化以及降低活化的Caspase3表达来抵消上述影响，从而减少细胞凋亡和钙化。此外，PI3K抑制剂可减弱这些作用。我们的研究证明，细胞外酸性刺激在Gas6/Axl或PI3K/Akt信号通路中对大鼠VSMC钙化和凋亡的抑制起至关重要的作用。
