Expression of IGFBP-3 in rat myocardial fibrosis and activation and proliferation of cardiac fibroblasts

Acta Universitatis Medicinalis Anhui 2020 02 v.55 263-268     font:big middle small

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Authors:Song Jiannan; Tao Hui; Ding Jifei

Keywords:IGFBP-3;myocardial fibrosis;cardiac fibroblasts;type Ⅰ collagen;proliferation;TGF-β1

DOI:10.19405/j.cnki.issn1000-1492.2020.02.021

〔Abstract〕 Objective To investigate the expression changes of insulin-like growth factor binding protein-3(IGFBP-3) in rat myocardial fibrosis and cardiac fibroblasts(CFs) activation and proliferation.Methods Forty SD rats were randomly divided into model group and control group. The model group rats were subcutaneously injected with isoproterenol to establish a model of myocardial tissue fibrosis. Transforming growth factor β1(TGF-β1) was used to stimulate the CFs of neonatal rats to make them proliferate and activate as a model group. The control group was CFs that were cultured normally without any stimulation. The rat myocardial tissue fibrosis model was used to detect pathological changes using HE and Masson staining, CCK-8 was used to determine the degree of CFs proliferation and activation, and qRT-PCR and Western blot were used to detect IGFBP-3 and α-smooth muscle actin(α-SMA) and type I collagen procollagen A1(COL1 A1) mRNA and protein expression.Results Compared with the control group,myocardial tissue collagen fibers proliferated and myocardial cells were disordered in the animal model group. CFs stimulated by TGF-β1 in the cell model group had significant proliferation and activation. Compared with the control group,the protein and mRNA expressions of IGFBP-3,α-SMA and COL1 A1 were significantly increased in the animal and cell model groups. Conclusion The expression of IGFBP-3 in fibrotic myocardium and CFs stimulated by TGF-β1 is significantly increased,suggesting that IGFBP-3 may promote or inhibit myocardial fibrotic lesions,which may be helpful to explore the pathological mechanism of myocardial fibrosis.