Overexpression of lncRNA GAS5 attenuates cardiac fibrosis through regulating PTEN/MMP-2 signal pathway in mice

H.-L. Liu, C.-H. Chen, Y.-J. Sun

Department of Cardiology, Lianshui County People’s Hospital, Huai’an China. haoqiaowo840301@163.com

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• Cardiology

OBJECTIVE: The present study aimed at investigating the effect and mechanism of lncRNA Growth Arrest-Specific 5 (GAS5) in cardiac fibrosis induced by isoproterenol (ISO) in vivo.
MATERIALS AND METHODS: The C57BL/6 mice were injected subcutaneously with ISO to induce cardiac fibrosis and injected intracoronary with lentivirus pcDNA-GAS5. After 3 weeks, cardiac function was detected by echocardiography. The interstitial collagen volume was stained by Masson trichrome. The expression of GAS5 was measured by Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR). The expressions of phosphatase and tensin homologue (PTEN), matrix metalloprotease-2 (MMP-2), α-smooth muscle actin (α-SMA), and collagen I protein were measured by Western blot.
RESULTS: Our results indicated that the expression of GAS5 was significantly down-regulated in the fibrotic myocardium. Overexpression of GAS5 after injection with pcDNA-GAS5 could attenuate cardiac fibrosis and improve cardiac function through increasing the expression of PTEN and decreasing the expression of MMP-2, α-SMA, and collagen I.
CONCLUSIONS: Overexpression of GAS5 could attenuate cardiac fibrosis induced by ISO. The molecular mechanism was associated with the regulation of PTEN/MMP-2 signaling pathway.

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