JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2012, Vol. 50 ›› Issue (11): 43-47.

• Articles • Previous Articles     Next Articles

TWEAK promotes expressions of collagen I and matrix metalloproteinase1
in rat cardiac fibroblasts via P38MAPK pathway

WANG Qi-lei1, REN Man-yi2, WANG De-jin1, XU Dong-ling1,
DU Yi-meng1, WANG Xu-ping3, SUI Shu-jian1   

  1. 1. Department of Cardiology， the Second Hospital of Shandong University, Jinan 250033,  China;
    2. Department of Cardiology, Shandong Provincial Chest Hospital, Jinan 250133, China;
    3． Department of Cardiology, Qilu Hospital of Shandong University, Key Laboratory of Cardiovascular Remodeling and
    Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Jinan 250012, China
  • Received:2012-03-29 Online:2012-11-10 Published:2012-11-10

PDF (PC)

347

Abstract:

Objective   To investigate the mechanism and effects of tumor necrosis factor-like inducer of apoptosis (TWEAK) on expressions of collagen I and matrix metalloproteinase1(MMP-1) in cardiac fibroblasts(CFs). Methods   Cultured CFs from neonatal Wistar rats were treated with the recombinant human TWEAK and the P38MAPK specific inhibitor(SB203580). CFs were divided into 3 groups: ① the control group: CFs were cultured without any stimulus; ② the TWEAK group: CFs were incubated with 100ng/mL TWEAK; ③ the TWEAK+SB203580 group: CFs were incubated with 100ng/mL TWEAK+SB203580. The CFs proliferation was examined by MTT, and expressions of collagen Ⅰ-and phosphor-P38MAPK protein were detected by Western blot. qRT-PCR was used to detect the collagen Ⅰ mRNA level. ELASA was used to detect the concentration of MMP1 in CFs cell-culture supernatant. Results   TWEAK promoted the proliferation of the CFs and expressions of collagen Ⅰ and phosphor-P38MAPK protein. The expressions of collagen Ⅰ mRNA and MCP-1 were up regulated due to TWEAK. P38MAPK specific inhibitor (SB203580) could inhibit the proliferation of CFs. P38MAPK specific inhibitor (SB203580) could partially inhibit expressions of collagens Ⅰ mRNA , collagens Ⅰ protein, phosphor-P38MAPK protein and MMP-1. Conclusion   TWEAK can promote expressions of collagen Ⅰ and MMP-1 in rat cardiac fibroblasts via P38MAPK pathway.

Key words: TWEAK; Cardiac fibroblasts; P38MAPK; Collagen I; MMP-1

CLC Number: 

  • R542.2
[1] SHEN Xiao-qian1, ZHANG Wen-dong2, HE Yuan-liu3, CONG Xiao4, SU Guo-hai4, HAO En-kui1. Research on cardiac dysfunction induced by trastuzumab and the possible mechanisms [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2013, 51(12): 11-14.
[2] KAN Li-li1, JIANG Fang-guo1, AN Feng-shuang2. Effect and expression of GRK2 on collagen synthesis in myocardial fibrosis rat model [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2013, 51(9): 22-25.
[3] WANG Fu1, LIU Shan-wen1, LI Bin2, GENG Hai-hua3, SUN Shuai1, LI Rui1, XIAO Jie1， JI Xiao-ping1. Protective effects of rhEPO on oxidative stress damage in cardiomyocytes and on heart after myocardial infarction [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2013, 51(7): 1-5.
[4] SUO Fei1, HU He-sheng2, XUE Mei2, WANG Ye1, XUAN Yong-li1, YAN Su-hua2 . Relationship between neurturin dynamic expression after myocardial infarction and cardiac vagal neural remodeling [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2013, 51(5): 1-5.
[5] ZHAO Li-xiang， WU Xin-ning， WANG Xi， LI Na， CHEN Tong-shuai, LIU Jun-ni， BU Pei-li. Effects of NAD on the mRNA expression of collagen  type I induced by Angiotensin II in cardiac fibroblasts [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2013, 51(3): 1-5.
[6] LU Guan-yan1, CUI Bin2, LIU Zhong-liang3, LI Yu-tang4, LIU Xue-fei3, MA Xiao-jing1, ZHU Gui-yue1, YUAN Hai-tao1. Valsartan alters the balance of Th17 cells to regulatory T cells in chronic viral  myocarditis [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2013, 51(2): 1-.
[7] WANG De-jin1， REN Man-yi2， CHEN Hui-na1， WANG Xu-ping3， SUI Shu-jian1. Tumor necrosis factor-like weak inducer of apoptosis promotes expression of matrix metalloproteinase 9 in rat cardiac fibroblasts via the nuclear factor-κB pathway [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2011, 49(11): 13-17.
[8] KAN Li-li1,2， AN Feng-shuang2. Evaluation of E/E′ on left ventricular diastolic function affected by  drug-treatment in the patients with hypertrophic cardiomyopathy [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2011, 49(7): 105-108.
[9] MA Li-na1, YAO Min-qiang2, WANG Pei-xian1. Echocardiographic evaluation on cardiac structure and function in patients with symptomatic alcoholic cardiomyopathy [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2011, 49(1): 82-85.
[10] . Prevalence of Fabry disease in patients with  hypertrophic cardiomyopathy [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2010, 48(3): 116-119.
[11] . Quantitative analysis of cardiac troponin T and the risk factors of myocardial infarction [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2009, 47(11): 114-117.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
No Suggested Reading articles found!
Copyright 2018 © Editorial office of Journal of Shandong University (Health Sciences)
Supported by Beijing Magtech Co.Ltd