JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2016, Vol. 54 ›› Issue (5): 23-28.doi: 10.6040/j.issn.1671-7554.0.2016.212

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Tumor necrosis factor-like weak inducer of apoptosis promotes expression of matrix metalloproteinase 2 and collagen Ⅰ in rat cardiac fibroblasts via the ERK1/2 signaling pathway

JU Yuanyuan1, REN Manyi2, LI Rui1, ZHAO Mengmeng1, SUI Shujian1   

  1. 1. Department of Cardiology, Second Hospital of Shandong University, Jinan 250033, Shandong, China;
    2. Department of Cardiology, Qianfoshan Hospital Affiliated to Shandong University, Jinan 250014, Shandong, China
  • Received:2016-03-03 Online:2016-05-16 Published:2016-05-16

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Abstract: Objective To explore the mechanism of tumor necrosis factor-like weak inducer of apoptosis(TWEAK)mediating the expression of MMP2 and collagen Ⅰ in cultured neonatal rat cardiac fibroblasts(CFs). Methods CFs were isolated and cultured using trypsin enzyme digestion technique. The protein expression of phosphorylated-ERK(p-ERK1/2)was detected with Western blotting, and then the optimal interventional concentration and duration of rhTWEAK and inhibitor PD98059 on ERK1/2 pathway in CFs were determined. The protein and mRNA expressions of MMP2 and collagen Ⅰ were investigated subsequently with real-time PCR(RT-PCR)and Western blotting. The effects of different treatments on cell proliferation were assessed with methyl thiazolyl tetrazolium(MMT). Results The 100 μg/L TWEAK significantly upregulated the protein expression of p-ERK1/2, improved the expressions of MMP2 and collagen Ⅰ at the transcriptional and translational level, and promoted cell proliferation. PD98059 inhibited the protein and mRNA expressions of MMP2 and collagen Ⅰ as well as the proliferation of CFs by blocking ERK1/2 signaling pathway. Conclusion TWEAK promotes the expression of MMP2 and collagen Ⅰ in CFs via ERK1/2 signaling pathway.

Key words: Tumor necrosis factor-like weak inducer of apoptosis, Collagen Ⅰ, Matrix metalloproteinase 2, Extracellular signal-regulated kinase 1/2

CLC Number: 

  • R542.2
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