PLGF参与Ang II诱导的心脏成纤维细胞激活

 目的：探讨胎盘生长因子（PLGF）在血管紧张素II（Ang II）激活心脏成纤维细胞(CFs)中的表达及其作用。方法：原代分离培养并鉴定新生SD大鼠CFs。蛋白免疫印迹检测α-平滑肌肌动蛋白（α-SMA）、PLGF和磷酸化ERK1/2(p-ERK1/2)，免疫荧光观察α-SMA的表达，WST-1法检测细胞增殖，RT-PCR检测PLGF、I型和III型胶原蛋白的mRNA表达水平。结果：(1)Ang II组PLGF mRNA 表达明显高于对照组（P<0．01)，联用替米沙坦后，PLGF mRNA表达水平下降；Ang  II组PLGF蛋白表达水平高于对照组（P<0.05); (2)PLGF诱导CFs增殖及α-SMA蛋白表达增加（P<0.05）；PLGF干预CFs 60 min后，p-ERK1/2蛋白水平表达明显高于对照组（P<0.01)；(3)Ang II+anti-PLGF组与Ang II组比较，细胞增殖和α-SMA蛋白表达水平下降（P<0.05），I型和III型胶原蛋白mRNA表达水平亦下调（P<0.05）。结论：PLGF可能参与Ang II诱导的CFs增殖和纤维化过程。

Placental growth factor is involved in angiotensin II-induced cardiac fibroblast activation

AIM：To explore the role of placental growth factor (PLGF) in the process of angiotensin II (Ang II)-induced activation of cardiac fibroblasts (CFs). METHODS：Primary culture and identification of CFs from neonatal Sprague-Dawley rats were performed. The method of fluorescence immunocytochemistry was employed to observe the expression of alpha-smooth muscle actin (α-SMA). Real-time PCR and Western blotting were used to determine mRNA and protein levels. The cell proliferation was observed by WST-1 assay. RESULTS：Compared with control group, the PLGF expression at mRNA and protein levels in Ang II-treated CFs was significantly increased, whereas the mRNA expression of PLGF was decreased in the CFs treated with telmisartan and Ang II. Treatment with PLGF induced the proliferation of CFs and increased the protein expression of α-SMA. Treatment with PLGF for 60 min significantly increased the protein levels of p-ERK1/2 in the CFs. Compared with Ang II group, the proliferation of CFs was depressed and the protein expression of α-SMA was attenuated in Ang II+anti-PLGF group.The mRNA expression levels of type I and type III collagens were also down-regulated. CONCLUSION：PLGF might be involved in the process of Ang II-induced proliferation of CFs and fibrosis.