Jin He1, Xiaoyi Zhong1, Lin Zhao2, Hua Gan3. 1. Department of Nephrology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China. 2. Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China. zhaolincqmu@163.com. 3. Department of Nephrology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China. ghcqmu@sina.com.
Abstract
BACKGROUND: Vascular 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. METHODS: The 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-κB signaling pathways was investigated by Western blotting. RESULTS: EPO-induced calcium deposition in VSMCs and significantly potentiated calcification in CKD rats. Furthermore, EPO activated JAK2/STAT3/BMP-2 axis, NF-κB pathway and the pro-calcification effect of EPO was partially blocked by the STAT3 inhibitor (Cryptotanshinone) or NF-κB inhibitor (BAY 11-7082), respectively, in vitro. CONCLUSION: EPO could promote VSMCs calcification in vitro and in vivo and this effect may be achieved through the JAK2/STAT3/BMP-2 axis and NF-κB pathway.
BACKGROUND:Vascular calcification is common in chronic kidney disease (CKD) patients, while erythropoietin (EPO) is widely used in the treatment of renal anemia in CKDpatients, whether there is a link between the two is still not clear. METHODS: The primary rat vascular smooth muscle cells (VSMCs) and CKDrats 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-κB signaling pathways was investigated by Western blotting. RESULTS:EPO-induced calcium deposition in VSMCs and significantly potentiated calcification in CKDrats. Furthermore, EPO activated JAK2/STAT3/BMP-2 axis, NF-κB pathway and the pro-calcification effect of EPO was partially blocked by the STAT3 inhibitor (Cryptotanshinone) or NF-κB inhibitor (BAY 11-7082), respectively, in vitro. CONCLUSION:EPO could promote VSMCs calcification in vitro and in vivo and this effect may be achieved through the JAK2/STAT3/BMP-2 axis and NF-κB pathway.
Authors: T Akimoto; E Kusano; T Inaba; O Iimura; H Takahashi; H Ikeda; C Ito; Y Ando; K Ozawa; Y Asano Journal: Kidney Int Date: 2000-07 Impact factor: 10.612
Authors: Guanghong Jia; Ryan M Stormont; Deepak M Gangahar; Devendra K Agrawal Journal: Am J Physiol Heart Circ Physiol Date: 2012-07-13 Impact factor: 4.733