您的位置：山东大学 -> 科技期刊社 -> 《山东大学学报（医学版）》

山东大学学报（医学版） ›› 2016, Vol. 54 ›› Issue (8): 12-16.doi: 10.6040/j.issn.1671-7554.0.2015.1223

• • 上一篇    下一篇

p38 MAPK信号通路调控人主动脉平滑肌细胞Ⅰ型和Ⅲ型胶原的表达

王晓琳1,周元丽2,孙伟3,李莉1   

  1. 1.山东大学附属济南市中心医院心内科, 山东 济南 250013;2.山东大学附属济南市中心医院保健科, 山东 济南 250013;3.济南大学, 山东省医学科学院医学与生命科学学院, 山东 济南 250062
  • 收稿日期:2015-12-03 出版日期:2016-08-10 发布日期:2016-08-10
  • 通讯作者: 李莉. E-mail:lili74@medmail.com.cn E-mail:lili74@medmail.com.cn
  • 基金资助:
    国家自然科学基金青年科学基金(81200211);山东省重点研发计划(2015GGA01027);山东省优秀中青年科学家科研奖励基金(2012BSA01018);济南市科技明星计划(20120144)

p38 MAPK signaling pathway regulates the expressions of type Ⅰ and Ⅲ collagens in human aortic smooth muscle cells

WANG Xiaolin1, ZHOU Yuanli2, SUN Wei3, LI Li1   

  1. 1. Department of Cardiology, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, Shandong, China;
    2. Department of Health, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, Shandong, China;
    3. School of Medicine and Life Sciences, University of Jinan, Shandong Academy of Medical Sciences, Jinan 250062, Shandong, China
  • Received:2015-12-03 Online:2016-08-10 Published:2016-08-10

PDF (PC)

316

摘要： 目的 探讨p38 MAPK对人主动脉平滑肌细胞Ⅰ型和Ⅲ型胶原表达的影响。 方法 分别使用药理学抑制剂和siRNA干预细胞。药理学抑制剂试验细胞分为:(1) 正常对照组,平滑肌细胞完全培养基正常培养;(2) DMSO(p38 MAPK抑制剂溶剂)对照组,0.01% DMSO处理;(3) p38 MAPK抑制剂组,0.01% p38 MAPK抑制剂(20 mg/mL)处理。基因沉默试验细胞分为:(1) 静态对照组,平滑肌细胞完全培养基正常培养; (2) 阴性对照siRNA组,MACSfectin试剂转染阴性对照siRNA 48 h; (3) p38 MAPK siRNA组,MACSfectin试剂转染p38 MAPK siRNA 48 h。采用qRT-PCR法检测Ⅰ型和Ⅲ型胶原mRNA表达;采用Western blotting法检测Ⅰ型和Ⅲ型胶原蛋白表达以及p38 MAPK转染效率;荧光显微镜观察siRNA转染效率。 结果 与正常对照组相比,DMSO对照组细胞Ⅰ型和Ⅲ型胶原mRNA和蛋白表达无明显变化(P>0.05),p38 MAPK抑制剂组细胞Ⅰ型和Ⅲ型胶原mRNA和蛋白表达显著降低(P<0.05)。与静态对照组相比,阴性对照siRNA组细胞Ⅰ型和Ⅲ型胶原mRNA和蛋白表达无明显变化(P>0.05),p38 MAPK siRNA组细胞Ⅰ型和Ⅲ型胶原mRNA和蛋白表达显著降低(P<0.05)。 结论 p38 MAPK信号通路调控人主动脉平滑肌细胞Ⅰ型和Ⅲ型胶原的表达。

关键词: Ⅰ型胶原, p38 MAPK, Ⅲ型胶原, 人主动脉平滑肌细胞

Abstract: Objective To investigate the effects of p38 MAPK on the expressions of type Ⅰ and type Ⅲ collagens in human aortic smooth muscle cells(HASMCs). Methods HASMCs were treated with inhibitors and siRNAs respectively. Inhibitor test cells were divided into 3 groups: (1) normal control group(cells were cultured in smooth muscle cell complete medium); (2) DMSO control group(cells were treated with 0.01% DMSO); (3) p38 MAPK inhibitor group(cells were treated with 0.01% p38 MAPK inhibitor(20 mg/mL). Gene silencing test cells were divided into 3 groups: (1) static control group(cells were cultured in smooth muscle cell complete medium); (2) negative control siRNA group(cells were transfected with negative control siRNAs for 48 h using MACSfectin reagent); (3) p38 MAPK siRNA group(cells were transfected with p38 MAPK siRNAs for 48 h using MACSfectin reagent). The mRNA expressions 山 东 大 学 学 报 (医 学 版)54卷8期 -王晓琳,等.p38 MAPK信号通路调控人主动脉平滑肌细胞Ⅰ型和Ⅲ型胶原的表达 \=- of type Ⅰ and Ⅲ collagens were detected by qRT-PCR, and the protein expressions were detected by Western blotting. The siRNAs transfection efficiency was observed with fluorescence microscope. Results Compared with the normal control group, the mRNA and protein expressions of type Ⅰ and Ⅲ collagens were not obviously changed in the DMSO control group(P>0.05), while the expressions decreased significantly in the p38 MAPK inhibitor group(P<0.05). Compared with the static control group, the mRNA and protein expressions of type Ⅰ and Ⅲ collagens were not obviously changed in the negative control siRNA group(P>0.05), while the expressions decreased significantly in the p38 MAPK siRNA group(P<0.05). Conclusion p38 MAPK signaling pathway regulates the expressions of type Ⅰ and type Ⅲ collagens in HASMCs.

Key words: Type Ⅲ collagen, Human aortic smooth muscle cells, p38 MAPK, Type Ⅰ collagen

中图分类号: 

  • R541.4
[1] Kataoka Y, Puri R, Nicholls SJ. Inflammation, plaque progression and vulnerability: evidence from intravascular ultrasound imaging[J]. Cardiovasc Diagn Ther, 2015, 5(4): 280.
[2] Tavakoli S, Vashist A, Sadeghi MM. Molecular imaging of plaque vulnerability[J]. J Nucl Cardiol, 2014, 21(6): 1112-1128.
[3] Hopkins PN. Molecular biology of atherosclerosis[J]. Physiol Rev, 2013, 93(3): 1317-1542.
[4] Cargnello M, Roux PP. Activation and function of the MAPKs and their substrates, the MAPK-activated protein kinases[J]. Microbiol Mol Biol Rev, 2011, 75(1): 50-83.
[5] Muslin A. MAPK signalling in cardiovascular health and disease: molecular mechanisms and therapeutic targets[J]. Clin Sci(Lond), 2008, 115(7): 203-218.
[6] Fisk M, Gajendragadkar PR, Mäki-Petäjä KM, et al. Therapeutic potential of p38 MAP kinase inhibition in the management of cardiovascular disease[J]. Am J Cardiovasc Drug, 2014, 14(3): 155-165.
[7] Yu XH, Fu YC, Zhang DW, et al. Foam cells in atherosclerosis[J]. Clin Chim Acta, 2013, 424: 245-252.
[8] Li L, Zhang K, Cai XJ, et al. Adiponectin upregulates prolyl-4-hydroxylase alpha1 expression in interleukin 6-stimulated human aortic smooth muscle cells by regulating ERK 1/2 and Sp1[J]. PLoS One, 2011, 6(7): 22819. doi: 10.1371/journal.pone.0022819.
[9] Zhang K, Meng X, Kong J, et al. Simvastatin increases Prolyl-4-Hydroxylase α1 expression in atherosclerotic plaque and ox-LDL-stimulated human aortic smooth muscle cells via p38 MAPK and ERK1/2 signaling[J]. J Mol Cell Cardiol, 2013, 65: 43-50.
[10] Cuadrado A, Nebreda A. Mechanisms and functions of p38 MAPK signaling[J]. Biochem J, 2010, 429(3): 403-417.
[11] Osman N, Ballinger ML, Dadlani HM, et al. p38 MAP kinase mediated proteoglycan synthesis as a target for the prevention of atherosclerosis[J]. Cardiovasc Hematol Disord Drug Targets, 2008, 8(4): 287-292.
[12] Bäck M, Hansson GK. Anti-inflammatory therapies for atherosclerosis[J]. Nat Rev Cardiol, 2015, 12(4): 199-211.
[1] 陆衡,刘延国,李曙光,陈晓康,田琦,衣翠华,王秀问. YKL-40对卵巢癌SKOV-3细胞迁移能力的影响[J]. 山东大学学报（医学版）, 2017, 55(1): 33-38.
[2] 巨媛媛,任满意,李睿,赵萌萌,隋树建. TWEAK通过ERK1/2通路促进大鼠心肌成纤维细胞MMP2与Ⅰ型胶原表达[J]. 山东大学学报（医学版）, 2016, 54(5): 23-28.
[3] 张锋, 戴杰, 任灵飞, 蒋颂瑶, 施更生. 纯钛钛片表面不同生物大分子涂层的比较研究[J]. 山东大学学报（医学版）, 2015, 53(8): 38-43.
[4] 商睿1,2，唐梦熊2,3，刘琳1,2，丁文渊2,3，郝盼盼2,3，陈玉国2,3. ALK7在高糖诱导的心肌成纤维细胞转化及Ⅰ型胶原合成中的作用[J]. 山东大学学报(医学版), 2013, 51(8): 1-6.
[5] 马敏1,张亮2,邵光峰1,张磊1，刘玉强1. 梗阻性肾病血清中Ⅲ型胶原水平与肾功能改变的相关性研究[J]. 山东大学学报(医学版), 2012, 50(3): 62-65.
[6] 王其磊1，任满意2，王德金1，徐冬玲1，杜贻萌1，王旭平3，隋树建1. TWEAK通过P38MAPK途径促进大鼠心肌成纤维细胞Ⅰ型胶原和MMP-1的表达[J]. 山东大学学报(医学版), 2012, 50(11): 43-47.
[7] 郭雪峰1,张继东1,姜红2,王博1,任敏1,冯利1. 芩丹胶囊对高血压大鼠血管壁Ⅰ型胶原蛋白与mRNA表达的影响[J]. 山东大学学报(医学版), 2010, 48(8): 18-21.
[8] 唐梦熊1,2,吕瑞娟1,2,钟明2,3,张运2,3,张薇2,3,陈玉国1,2. Tribble 3在高糖促进心肌成纤维细胞合成Ⅰ型胶原中的作用[J]. 山东大学学报(医学版), 2010, 48(11): 20-.
[9] 张亮1，刘玉强1，李远2，殷钢1，孟凡伟3，柳豪4，王传运5. 梗阻性肾病肾纤维化与血清中Ⅲ型胶原变化的相关性研究[J]. 山东大学学报(医学版), 2009, 47(12): 29-32.
[10] 田红,王淑娟,李洪佳,董亮. 转录因子T-bet/GATA-3诱导哮喘模型中α-SMA和Ⅰ型胶原高表达的实验研究[J]. 山东大学学报(医学版), 2007, 45(11): 1110-1113.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
No Suggested Reading articles found!
版权所有 © 2018 《山东大学学报(医学版)》编辑部　
地址:山东大学科技期刊社（济南市历城区山大南路27号山东大学中心校区明德楼B座721室） 电话: 0531-88366918 E-mail: xbyxb@sdu.edu.cn
本系统由北京玛格泰克科技发展有限公司设计开发