The Effects of RBP4 and Vitamin D on the Proliferation and Migration of Vascular Smooth Muscle Cells via the JAK2/STAT3 Signaling Pathway.
The Effects of RBP4 and Vitamin D on the Proliferation and Migration of Vascular Smooth Muscle Cells via the JAK2/STAT3 Signaling Pathway.
复制标题
RBP4和维生素D通过JAK2/STAT3信号通路对血管平滑肌细胞增殖和迁移的影响
DOI：
10.1155/2022/3046777
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发表时间：
2022
影响因子：
--
通讯作者：
Liu Q
中科院分区：
文献类型：
--
作者：
Zhou W;Wang W;Yuan XJ;Xiao CC;Xing Y;Ye SD;Liu Q
血管平滑肌细胞（VSMCs）的异常增殖和迁移是糖尿病动脉粥样硬化进程发展的主要原因之一。我们研究的目的是评估视黄醇结合蛋白4（RBP4）在VSMCs增殖和迁移中的作用以及维生素D对相关机制的抑制作用。在体内实验中，大鼠被随机分为6组：对照组、糖尿病大鼠组、糖尿病动脉粥样硬化大鼠组（糖尿病大鼠腹腔注射RBP4）、用0.075μg·kg⁻¹·d⁻¹维生素D治疗的糖尿病动脉粥样硬化大鼠组、用0.15μg·kg⁻¹·d⁻¹维生素D治疗的糖尿病动脉粥样硬化大鼠组以及用0.3μg·kg⁻¹·d⁻¹维生素D治疗的糖尿病动脉粥样硬化大鼠组。我们发现糖尿病动脉粥样硬化大鼠中JAK2、STAT3、细胞周期蛋白D1（cyclinD1）和Bcl - 2的水平升高，补充维生素D后这些升高的情况得到改善。此外，为了研究潜在的分子机制，分别在有RBP4和无RBP4的情况下用葡萄糖培养细胞，同时采用不同浓度和不同干预时间的维生素D。转染RBP4过表达质粒的细胞中VSMCs的增殖和迁移增强，JAK2、STAT3、cyclinD1和Bcl - 2的水平升高。而且，检测到补充维生素D可降低JAK2、STAT3、cyclinD1和Bcl - 2的表达，并抑制由RBP4/JAK2/STAT3信号通路引起的VSMCs异常增殖。RBP4可促进VSMCs的增殖和迁移，并通过调节JAK2/STAT3信号通路促进糖尿病大血管病变的发展。补充维生素D可抑制RBP4的这种机制。
Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) are one of the main causes of the development of diabetic atherosclerotic process. The aim of our study was to assess the role of RBP4 in the proliferation and migration of VSMCs and the inhibitory effect of vitamin D on the mechanisms. In an in vivo experiment, rats were randomly classified into 6 groups: the control group, diabetic rats, diabetic atherosclerotic rats (diabetic rats intraperitoneally injected with RBP4), diabetic atherosclerotic rats treated with 0.075 μg kg−1 d−1 vitamin D, 0.15 μg kg−1 d−1 vitamin D and 0.3 μg kg−1 d−1 vitamin D. We found that the levels of JAK2, STAT3, cylinD1, and Bcl-2 were increased in diabetic atherosclerotic rats, and these increases were improved after vitamin D supplementation. Furthermore, to investigate the underlying molecular mechanisms, cells were cultured with glucose in the presence of RBP4 and the absence of RBP4, respectively, and vitamin D of different concentrations and different intervention times was simultaneously adopted. The proliferation and migration of VSMCs was enhanced and the levels of JAK2, STAT3, cyclinD1, and Bcl-2 were increased in the cells transfected with RBP4 overexpression plasmid. Moreover, vitamin D supplementation was detected to lower the expressions of JAK2, STAT3, cyclinD1, and Bcl-2 and inhibit the abnormal proliferation of VSMCs caused by the RBP4/JAK2/STAT3 signaling pathway. RBP4 can promote the proliferation and migration of VSMCs and contributes to the development of diabetic macroangiopathy via regulating the JAK2/STAT3 signaling pathway. This mechanism of RBP4 can be inhibited by vitamin D supplementation.
影响因子：
3.7
作者：
Gao D;Hao G;Meng Z;Ning N;Yang G;Liu Z;Dong X;Niu X
通讯作者：
Niu X
抑制 JAK2/STAT3 信号传导可减少大鼠颈总动脉端到端动脉吻合诱导的细胞增殖
影响因子：
3.7
作者：
Zhao J;Zhang M;Li W;Su X;Zhu L;Hang C
通讯作者：
Hang C
影响因子：
2.4
作者：
Kawaguchi, Riki;Zhong, Ming;Kassai, Miki;Ter-Stepanian, Mariam;Sun, Hui
通讯作者：
Sun, Hui