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

Biosci Rep. 2021 Feb 26;41(2):BSR20204099. doi: 10.1042/BSR20204099.

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.

Keywords: ICAM-1; diabetic nephropathy; high-glucose; lncRNA SNHG15; miR-141.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Child
  • Diabetic Nephropathies / genetics*
  • Diabetic Nephropathies / pathology*
  • Disease Progression
  • Gene Knockdown Techniques*
  • Glomerular Mesangium / metabolism
  • Glomerular Mesangium / pathology
  • Humans
  • Intercellular Adhesion Molecule-1 / genetics*
  • MicroRNAs / genetics*
  • RNA, Long Noncoding / genetics*

Substances

  • ICAM1 protein, human
  • MIRN141 microRNA, human
  • MicroRNAs
  • RNA, Long Noncoding
  • Intercellular Adhesion Molecule-1