崩解蛋白和金属蛋白酶与血小板反应蛋白基序1抑制剂修饰的骨髓间充质干细胞对心肌炎心肌纤维化的调节作用

Kexin Yuan, Peng Qi, Xiao Hao, Qingqing Hao, Pei Zhao
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摘要

本研究评估了ADAMTS-1抑制剂修饰的BMSC通过TGFβ1/MMP9/TIMP1通路和胶原代谢调节心肌炎心肌纤维化的机制。建立病毒性心肌炎(VMC)大鼠模型,将其随机分为对照组、载体组、抑制剂组、载体和抑制剂组,然后通过RT-PCR分析心房组织CVF%、ADAMTS-1水平,通过IHC分析TGFβ1、MMP9和TIMP1水平。ADAMTS-1mRNA水平在对照组最高,在抑制剂组最低。每一组都有过度的纤维化。抑制剂组、载体和抑制剂组心肌纤维化程度降低。炎症细胞的数量也显著减少。没有或有零星的商城灶性坏死。与对照组相比,治疗组的TGFβ1、MMP9和TIMP1水平显著降低,抑制剂组、载体和抑制剂组的变化更为显著。ADAMTS-1抑制剂修饰的BMSC抑制了VMC大鼠的胶原代谢,从而改善了心肌纤维化,其可能机制是通过调节TGFβ1/MMP9/TIMP1信号通路。
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Bone Marrow Mesenchymal Stem Cell Modified with A Disintegrin and Metalloproteinase with Thrombospondin Motifs 1 Inhibitor Regulates Myocardial Fibrosis in Myocarditis
This study assesses the mechanism of BMSC modified with ADAMTS-1 inhibitor in regulating the myocardial fibrosis in myocarditis through TGFβ1/MMP9/TIMP1 pathway and collagen metabolism. Model of viral myocarditis (VMC) rats was established and then assigned into control set, carrier set, inhibitor set and carrier and inhibitor set randomly followed by analysis of CVF% in atrial tissue, ADAMTS-1 level by RT-PCR and TGFβ1, MMP9 and TIMP1 level by IHC. ADAMTS-1 mRNA level in control set was highest and lowest in inhibitor set. There was fibrosis in every set inordinately. The degree of myocardial fibrosis was reduced in inhibitor set and carrier and inhibitor set. The quantity of inflammatory cells was also reduced significantly. There was no or sporadic mall focal necrosis. The level of TGFβ1, MMP9 and TIMP1 in the treated three sets was significant decreased compared with control set with more significant changes in the inhibitor set and carrier and inhibitor set. Collagen metabolism in VMC rats was restrained by BMSC modified with ADAMTS-1 inhibitor and therefore the myocardial fibrosis was ameliorated with the possible mechanism being through regulation of the TGFβ1/MMP9/TIMP1 signaling pathway.
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