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长链非编码RNA MALAT1在糖尿病胃轻瘫中上调,并参与高糖诱导的人胃平滑肌细胞的细胞过程。

LncRNA MALAT1 is up-regulated in diabetic gastroparesis and involved in high-glucose-induced cellular processes in human gastric smooth muscle cells.

作者信息

Gong Yaoyao, Zhu Ying, Zhu Boqian, Si Xinmin, Heng Ding, Tang Yurong, Sun Xiaomeng, Lin Lin

机构信息

Department of Gastroenterology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.

Department of Cardiology, Zhongda Hospital, Southeast University, Nanjing, China.

出版信息

Biochem Biophys Res Commun. 2018 Feb 5;496(2):401-406. doi: 10.1016/j.bbrc.2018.01.038. Epub 2018 Jan 6.

Abstract

Recent years, widespread long non-coding RNAs (lncRNAs) were identified and known as regulator of gene expression. Diabetic gastroparesis (DGP) is one of the most common chronic complications of diabetes mellitus. There was no research reported the role of lncRNAs in DGP. In this study, we firstly established a rat model of DGP by STZ injection. Then, we detected the expression of MALAT1 and found that expression of MALAT1 was up-regulated in rat model of DGP, comparing to the control group (P < .01). Furthermore, we revealed that MALAT1 expression was increased in the samples from diabetic patients with DGP symptoms, in comparison with the control. In addition, we demonstrated that the inhibition of MALAT1 increased the expression of α-SMA and SM myosin heavy chains, reduced the cell viability, inhibited the potential of cell migration and induced cell apoptosis in human gastric smooth muscle cells (SMCs). Ultimately, we found that the regulation of MALAT1 expression modulated the function of high-glucose stimulation in human gastric SMCs. Therefore, our study firstly indicated that MALAT1 was up-regulated in DGP and played an important role in the pathogenesis of DGP.

摘要

近年来,广泛存在的长链非编码RNA(lncRNAs)被鉴定出来,并被认为是基因表达的调节因子。糖尿病胃轻瘫(DGP)是糖尿病最常见的慢性并发症之一。尚无研究报道lncRNAs在DGP中的作用。在本研究中,我们首先通过注射链脲佐菌素(STZ)建立了DGP大鼠模型。然后,我们检测了MALAT1的表达,发现与对照组相比,DGP大鼠模型中MALAT1的表达上调(P<0.01)。此外,我们发现与对照组相比,有DGP症状的糖尿病患者样本中MALAT1表达增加。另外,我们证明抑制MALAT1可增加人胃平滑肌细胞(SMCs)中α-SMA和SM肌球蛋白重链的表达,降低细胞活力,抑制细胞迁移能力并诱导细胞凋亡。最终,我们发现MALAT1表达的调节可调节高糖刺激下人胃SMCs的功能。因此,我们的研究首次表明MALAT1在DGP中上调,并在DGP的发病机制中起重要作用。

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