1-磷酸鞘氨醇受体1参与晚期糖基化终产物引起的血管平滑肌细胞增殖和迁移
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(1.南方医科大学珠江医院教务处,广东省广州市 510280;2.南方医科大学基础医学院病理生理学教研室 广东省医学休克微循环重点实验室,广东省广州市 510515;3.南方医科大学附属第三医院创伤外科中心,广东省广州市 510500)

作者简介:

袁咏军,硕士,研究方向为晚期糖基化终产物介导血管病变的机制,E-mail为444959672@qq.com。通信作者黄巧冰,博士,教授,博士研究生导师,研究方向为糖尿病微血管并发症的发生机制,E-mail为bing@smu.edu.cn。

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基金项目:

国家自然科学基金面上项目(81870210);广东省自然科学基金团队项目(S2013030013217)


Sphingosine 1-phosphate receptor 1 participates in the proliferation and migration of vascular smooth muscle cells induced by advanced glycation end products
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1.Teaching Office, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong 510280, China;2.Department of Pathophysiology, School of Basic Medicine, Southern Medical University & Guangdong Provincial Key Laboratory of Shock and Microcirculation, Guangzhou, Guangdong 510515, China;3.Trauma Surgery Center, the Third Affiliated Hospital of Southern Medical University, Guangzhou, Guangdong 510500, China)

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    摘要:

    目的 观察1-磷酸鞘氨醇受体1(S1PR1)在晚期糖基化终产物(AGE)引起的血管平滑肌细胞增殖和迁移中的作用。方法 培养人脐动脉平滑肌细胞(HUASMC),葡萄糖与牛血清白蛋白(BSA)孵育法获得AGE-BSA,分为对照组、BSA组和AGE-BSA组,采用CCK-8实验检测平滑肌细胞增殖能力,采用细胞划痕和Transwell实验检测平滑肌细胞迁移能力,并进一步观察BSA和AGE-BSA在有或无S1PR1拮抗剂VPC23019/激动剂SEW2871预处理后的细胞增殖和迁移。结果 与对照组比较,BSA和AGE-BSA均能诱导HUASMC增殖和迁移,AGE-BSA的作用比BSA更加显著(P<0.05);S1PR1拮抗剂VPC23019可以明显抑制BSA和AGE-BSA诱导的HUASMC增殖和迁移;S1PR1激动剂SEW2871本身就可以促进HUASMC增殖和迁移,并且进一步促进BSA诱导的HUASMC增殖和迁移,而对AGE-BSA诱导的HUASMC增殖和迁移没有进一步的促进作用。结论 血浆白蛋白本身对平滑肌细胞的增殖具有促进作用,糖基化修饰的白蛋白这一作用更加明显;S1PR1的激活参与了BSA和AGE-BSA促进平滑肌细胞增殖和迁移,AGE-BSA对S1PR1的激活作用更加显著。

    Abstract:

    Aim To observe the effect of sphingosine 1-phosphate receptor 1(S1PR1) on vascular smooth muscle cell proliferation and migration induced by advanced glycation end products (AGE). Methods Human umbilical artery smooth muscle cells (HUASMC) were cultured, and AGE-BSA was obtained by incubating with glucose and albumin. Cells were divided to control, BSA and AGE-BSA treated group. CCK-8 kit was used to detect the proliferation of smooth muscle cells, cell scratching and Transwell assays were applied to study the migration of smooth muscle cells. S1PR1 antagonist VPC23019 or agonist SEW2871 were used to investigate the role of S1PR1 in the proliferation and migration of human umbilical artery smooth muscle cells with BSA or AGE-BSA treatment. Results Compared with control group, BSA and AGE-BSA induced proliferation and migration of human umbilical artery smooth muscle cells, and the effect of AGE-BSA was more significant than that of BSA (P<0.05). VPC23019, an antagonist of S1PR1, significantly attenuated the proliferation and migration of human umbilical artery smooth muscle cells induced by BSA and AGE-BSA. The S1PR1 agonist SEW2871 itself promoted the proliferation and migration of human umbilical artery smooth muscle cells, and further enhanced the proliferation and migration of human umbilical artery smooth muscle cells induced by BSA, but had no further promotion effect on the proliferation and migration of human umbilical artery smooth muscle cells induced by AGE-BSA. Conclusions Plasma albumin itself can promote the proliferation and migration of smooth muscle cells, and the effect of glycosylated albumin is more remarkable. The activation of S1PR1 is involved in BSA and AGE-BSA-induced proliferation and migration of human umbilical artery smooth muscle cells, and the activation of S1PR1 by AGE-BSA was more significant.

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袁咏军,黄巧冰.1-磷酸鞘氨醇受体1参与晚期糖基化终产物引起的血管平滑肌细胞增殖和迁移[J].中国动脉硬化杂志,2021,29(10):845~850.

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  • 收稿日期:2020-07-24
  • 最后修改日期:2020-09-15
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  • 在线发布日期: 2021-10-13