JAK2/STAT3/BMP-2 axis and NF-B pathway are involved in erythropoietin-induced calcification in rat vascular smooth muscle cells
JAK2/STAT3/BMP-2 axis and NF-B pathway are involved in erythropoietin-induced calcification in rat vascular smooth muscle cells
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DOI：
10.1007/s10157-018-1666-z
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发表时间：
2019-04-01
影响因子：
2.3
通讯作者：
Gan, Hua
中科院分区：
文献类型：
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作者：
He, Jin;Zhong, Xiaoyi;Gan, Hua
研究背景血管钙化是慢性肾脏病（CKD）患者常见的现象，而促红细胞生成素（EPO）被广泛用于治疗CKD患者的肾性贫血，两者之间是否存在联系尚不清楚。JAK 2/STAT 3/BMP-2轴和NF-B信号通路的激活进行了调查通过Western blotting. ResultsEPO诱导的VSMCs的钙沉积和显着增强在CKD大鼠钙化。EPO在体外可激活JAK 2/STAT 3/BMP-2轴和NF-B通路，其促钙化作用可分别被STAT 3抑制剂隐丹参酮（Cryptotanshinone）和NF-B抑制剂BAY 11-7082部分阻断。
BackgroundVascular calcification is common in chronic kidney disease (CKD) patients, while erythropoietin (EPO) is widely used in the treatment of renal anemia in CKD patients, whether there is a link between the two is still not clear.MethodsThe primary rat vascular smooth muscle cells (VSMCs) and CKD rats were treated with EPO and the calcium deposition was observed by alizarin red staining, von Kossa staining and calcium quantification. Activation of JAK2/STAT3/BMP-2 axis and NF-B signaling pathways was investigated by Western blotting.ResultsEPO-induced calcium deposition in VSMCs and significantly potentiated calcification in CKD rats. Furthermore, EPO activated JAK2/STAT3/BMP-2 axis, NF-B pathway and the pro-calcification effect of EPO was partially blocked by the STAT3 inhibitor (Cryptotanshinone) or NF-B inhibitor (BAY 11-7082), respectively, in vitro.ConclusionEPO could promote VSMCs calcification in vitro and in vivo and this effect may be achieved through the JAK2/STAT3/BMP-2 axis and NF-B pathway.