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目的研究核不均一核糖蛋白A1(heterogeneous nuclear ribonucleoprotein A1,hnRNP A1)是否可以通过IκBα/NF-κB信号通路调控平滑肌细胞的钙化过程。方法分离培养原代人脐动脉血管平滑肌细胞(human umbilical artery smooth muscle cells,HUASMCs),构建pc DNA3.1-hnRNP A1真核表达质粒并转染HUASMCs,观察hnRNP A1对HUASMCs增殖和凋亡功能的影响。建立HUASMCs钙化模型,研究hnRNP A1在血管平滑肌钙化过程中的作用机制。结果 hnRNP A1表达水平在HUASMCs由收缩型转变为合成型的分化过程中显著上调,但hnRNP A1对HUASMCs细胞的增殖和凋亡功能无显著影响。无论是否给予H2O2刺激,hnRNP A1均可促进HUASMCs细胞形成钙化结节,其促进钙化的分子机制不是通过IκBα/NF-κB信号通路介导。结论本研究发现hnRNP A1在平滑肌细胞由收缩型向合成型转化的过程中表达上调,过表达hnRNP A1促进平滑肌细胞钙化。
Objective To investigate whether heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) regulates smooth muscle cell calcification via IκBα / NF-κB signaling pathway. Methods Primary human umbilical artery smooth muscle cells (HUASMCs) were isolated and cultured. The eukaryotic expression plasmid pcDNA3.1-hnRNP A1 was constructed and transfected into HUASMCs. The proliferation and apoptosis of HUASMCs were observed influences. The HUASMCs calcification model was established to study the mechanism of hnRNP A1 in calcification of vascular smooth muscle. Results The expression of hnRNP A1 was significantly up-regulated during the differentiation from HUASMCs to the synthetic ones. However, hnRNP A1 had no significant effect on the proliferation and apoptosis of HUASMCs. HnRNP A1 promoted the formation of calcified nodules in HUASMCs regardless of the stimulation of H2O2. The molecular mechanism of hnRNP A1 activation was not mediated by IκBα / NF-κB signaling pathway. Conclusion This study found that hnRNP A1 was up-regulated in the process of transforming smooth muscle cells from contractile to synthetic. Overexpression of hnRNP A1 promoted smooth muscle cell calcification.