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

Vascular biology (Bristol, England) Pub Date : 2022-09-30 Print Date: 2022-09-01 DOI:10.1530/VB-22-0006

Xusheng Zhang, Zhanjun Huang, Xiaorong Fan, Xiaoqing Tan, Chengzhi Lu, Jianshe Yang

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引用次数: 1

Abstract

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.

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尿皮质素II对钙化培养基诱导的大鼠外膜成纤维细胞钙化的分子机制和作用。

本研究旨在通过使用钙化模型评估尿皮质素II（UII）在体外血管钙化过程中的作用，检测大鼠外膜成纤维细胞（AF）向成骨细胞表型转化过程中相关标志物的mRNA和蛋白水平的变化，以阐明UII负责调节血管钙化和成骨细胞AF表型转化的主要信号转导途径，并证明UII是促进血管钙化的内源性因子，为临床调控血管钙化引起的相关疾病提供有效的实验依据。最后，我们成功构建了钙化细胞模型，发现UII是一种调节血管钙化的内源性物质，通过上调和下调BAX和BCL-2/BECLIN1（BECN1）水平来促进细胞凋亡和抑制自噬来调节血管钙化，并参与了Wnt/β-catenin信号通路。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Vascular biology (Bristol, England)

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13 weeks