SNHG15 knockdown inhibits diabetic nephropathy progression in pediatric patients by regulating the miR-141/ICAM-1 axis in vitro.

Jiewei Liu,Yanhong Zou,Ying Wang,Dongliang Cai,Tana Zhao

doi:10.1042/bsr20204099

Jiewei Liu, Yanhong Zou + Show 3 more

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https://doi.org/10.1042/bsr20204099

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Abstract

Long non-coding RNAs (lncRNAs) are confirmed to be involved in modulating diabetic nephropathy (DN). The present study is aimed to explore the regulatory mechanism of lncRNA small nucleolar RNA host gene 15 (SNHG15) on pediatric DN. Human glomerular mesangial cells (HGMCs) were exposed to high glucose (HG) to produce an in vitro model. The results showed that SNHG15 was remarkably up-regulated in pediatric DN tissues and HG-induced HGMCs. Functional experiments indicated that both silencing of SNHG15 and overexpression of miR-141 elevated the cell viability, and suppressed the inflammation in HG-induced HGMCs. SNHG15 was identified to be a lncRNA that could bind to miR-141, and ICAM-1 was a downstream target gene of miR-141. Both the low expression of miR-141 and high expression of ICAM-1 reversed the inhibiting effect of SNHG15 knockdown on inflammatory response, and the promoting effect on cell viability. To conclude, our study revealed that silencing of SNHG15 ameliorated the malignant behaviors of pediatric DN via modulating the miR-141/ICAM-1 axis in vitro.

Highlights

Diabetic nephropathy (DN) is a main and serious complication of diabetes mellitus (DM) [1,2]
We investigated the effects of long non-coding RNA (lncRNA) small nucleolar RNA host gene 15 (SNHG15) on the viability and inflammation of human glomerular mesangial cell (HGMC), and explored the regulatory mechanisms between SNHG15 and miR-141/Intercellular adhesion molecule-1 (ICAM-1) on pediatric DN
We found that SNHG15 expression was increased in high glucose (HG)-induced HGMCs compared with the NG controls. (Figure 1B, P

Summary

Introduction

Diabetic nephropathy (DN) is a main and serious complication of diabetes mellitus (DM) [1,2]. The pathological features of DN are in many ways and inflammation is one of the most common pathological factors [6,7]. Numerous researches have indicated that inflammation response in renal facilitates the development of DN [8,9]. Various therapies such as controlling blood glucose [10] and inflammation [11] for treating DN have been improved, the therapeutic effects remain disillusionary.

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