%A HAO Jia-le, XU Li-cong, HUANG Tian-peng, YU Yan, WANG Yao-yao, FAN Xiao-fang, GONG Yong-sheng, MAO Sun-zhong %T Effects of apolipoprotein E on proliferation of mouse pulmonary arterial smooth muscle cells induced by hypoxia %0 Journal Article %D 2019 %J CJAP %R 10.12047/j.cjap.5838.2019.090 %P 414-417 %V 35 %N 5 %U {http://manu37.magtech.com.cn/Jwk_jsyxkx/cjap/CN/abstract/article_148482.shtml} %8 2019-09-28 %X Objective: To investigate the effects of apolipoprotein E (apoE) on the proliferation of pulmonary arterial smooth muscle cells (PASMCs) induced by hypoxia. Methods: Primary culture of mouse PASMCs was prepared from male C57BL/6 mouse pulmonary artery by the method of tissue block anchorage. PASMCs were divided into four groups: normoxia group, normoxia with apoE administration group, hypoxia group and hypoxia with apoE administration group. The proliferation of PASMCs was observed by EdU incorporation. The protein levels of apoE, proliferating cell nuclear antigen (PCNA), protein kinase C (PKC) and phosphorylated protein kinase C (p-PKC) were analyzed by Western blot.Results: The percentage of PASMCs proliferation of hypoxia group was significantly higher than that of normoxia group by 64.7% (P<0.05), and the protein expression levels of PCNA and p-PKC of hypoxia group were up-regulated than those of normoxia group by 69.0% and 120.0%, while the protein expression of apoE was down-regulated by 51.0% (P<0.05), respectively. The percentage of PASMCs proliferation of hypoxia with apoE administration group was significantly lower than that of hypoxia group by 19.6% (P<0.05), and the protein expression levels of PCNA and p-PKC of hypoxia with apoE administration group were down-regulated than those of hypoxia group by 19.8% and 103.2% (P<0.05), respectively. There was no significant difference among each group in the protein expression of PKC, nor do there any significant difference between normoxia group and hypoxia group in the protein expression of p-PKC (P>0.05). Conclusion: ApoE can inhibit the proliferation of PASMCs induced by hypoxia, and the mechanism of its effect may be attributed to blocking PKC pathway.