MicroRNA-124a contributes to glucocorticoid resistance in acute-on-chronic liver failure by negatively regulating glucocorticoid receptor alpha

Ann Hepatol. 2020 Mar-Apr;19(2):214-221. doi: 10.1016/j.aohep.2019.08.007. Epub 2019 Oct 1.

Abstract

Introduction and objectives: Glucocorticoid resistance frequently associating with inflammation, may severely compromise the therapeutic effect of glucocorticoids. In this study, we aimed to investigate the regulation of glucocorticoid resistance by microRNA-124a (miR-124a) in patients with acute-on-chronic liver failure (ACLF).

Materials and methods: The miR-124a levels and glucocorticoid receptor alpha (GRα) expressions in peripheral blood monocytes and liver tissues were measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR), flow cytometry, and western blot analyses in the following four groups: healthy controls (HC), moderate chronic hepatitis B (CHB) patients, hepatitis B virus-related ACLF (HBV-ACLF) patients, and alcohol-induced ACLF (A-ACLF) patients. In addition, the serum miR-124a levels and multiple biochemical indices were determined. The effects of miR-124a transfection on GRα expression were assayed by qRT-PCR and western blotting in U937 and HepG2 cells stimulated with lipopolysaccharide (LPS).

Results: Compared with the CHB patients and HC, the miR-124a levels in HBV-ACLF and A-ACLF patients increased, while GRα expressions decreased. No significant differences in miR-124a levels and GRα expressions were observed between the HBV-ACLF and A-ACLF patients. For the ACLF patients, miR-124a level was negatively related to GRα expression in monocytes and positively correlated with the inflammatory factors such as interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α). In U937 and HepG2 cells, LPS stimulated miR-124a levels but inhibited GRα expressions; meanwhile, increasing miR-124a levels reduced GRα expressions, and inhibiting miR-124a levels increased GRα expressions.

Conclusions: This study provides evidence that GRα expression was negatively regulated by miR-124a, which primarily determines the extent of acquired glucocorticoid resistance in ACLF.

Keywords: Acute-on-chronic liver failure; Biomarker; Glucocorticoid resistance; MicroRNA-124a.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute-On-Chronic Liver Failure / drug therapy
  • Acute-On-Chronic Liver Failure / etiology
  • Acute-On-Chronic Liver Failure / metabolism*
  • Adult
  • Case-Control Studies
  • Drug Resistance / genetics
  • Female
  • Gene Expression Regulation
  • Gene Knock-In Techniques
  • Hep G2 Cells
  • Hepatitis B, Chronic / complications
  • Hepatitis B, Chronic / metabolism*
  • Humans
  • Interleukin-1beta / metabolism
  • Interleukin-6 / metabolism
  • Liver Diseases, Alcoholic / complications
  • Liver Diseases, Alcoholic / metabolism*
  • Male
  • MicroRNAs / genetics*
  • Middle Aged
  • Monocytes / metabolism
  • Receptors, Glucocorticoid / genetics*
  • Receptors, Glucocorticoid / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Necrosis Factor-alpha / metabolism
  • U937 Cells

Substances

  • IL1B protein, human
  • IL6 protein, human
  • Interleukin-1beta
  • Interleukin-6
  • MIRN124 microRNA, human
  • MicroRNAs
  • Receptors, Glucocorticoid
  • TNF protein, human
  • Tumor Necrosis Factor-alpha
  • glucocorticoid receptor alpha