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Molecular mechanisms and effects of urocortin II on rat adventitial fibroblast calcification induced by calcified medium

Xusheng Zhang

Xusheng Zhang Department of Cardiology, The First Central Clinical College of Tianjin Medical University, Tianjin, China
Department of Cardiology, Tianjin First Central Hospital, Tianjin, China
Department of Cardiology, Longgang People’s Hospital of Shenzhen, Shenzhen, Guangdong, China

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Zhanjun Huang

Zhanjun Huang Department of Cardiology, Longgang People’s Hospital of Shenzhen, Shenzhen, Guangdong, China

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Xiaorong Fan

Xiaorong Fan Department of Cardiology, Longgang People’s Hospital of Shenzhen, Shenzhen, Guangdong, China

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Xiaoqing Tan

Xiaoqing Tan Department of Cardiology, Longgang People’s Hospital of Shenzhen, Shenzhen, Guangdong, China

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Chengzhi Lu

Chengzhi Lu Department of Cardiology, The First Central Clinical College of Tianjin Medical University, Tianjin, China
Department of Cardiology, Tianjin First Central Hospital, Tianjin, China

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Jianshe Yang

Jianshe Yang Department of Nuclear Medicine, Shanghai Tenth People’s Hospital, Tongji University, Shanghai, China

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The present study aimed to assess the role of urocortin II (UII) in the process of vascular calcification in vitro by using a calcification model, to detect the changes in the mRNA and protein levels of associated markers in rat adventitial fibroblasts (AFs) during their phenotypic transformation to osteoblast cellsto clarify the main signal transduction pathway of UII responsible for regulating vascular calcification and AF phenotypic transformation of osteoblast cells, and to prove that UII was an endogenous factor promoting vascular calcification, so as to provide an effective experimental basis for the clinical regulation of related diseases caused by vascular calcification. Finally, we successfully constructed the calcified cell model, found that UII was an endogenous substance regulating vascular calcification, regulated the vascular calcification by promoting apoptosis and inhibiting autophagy through up- and downregulated BAX and BCL-2/BECLIN 1 (BECN1) level, and the Wnt/β-catenin signaling pathway was involved.