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Glucose stimulates microRNA-199 expression in murine pancreatic β-cells

Joao Pedro Werneck-de-Castro1,2, Manuel Blandino-Rosano1, Denise Hilfiker-Kleiner3

  • 1Division of Endocrinology, Diabetes, and Metabolism, University of Miami, Miller School of Medicine, Miami, Florida 33136.

The Journal of Biological Chemistry
|December 29, 2019
PubMed

Insights

High glucose levels acutely increase microRNA 199 (miR-199) expression in pancreatic beta cells. Glucose metabolism and calcium influx regulate miR-199 precursor expression, impacting beta cell function.

Area of Science:

  • Molecular Endocrinology
  • Metabolic Disease Research
  • Cellular Signaling

Background:

  • MicroRNA 199 (miR-199) negatively regulates pancreatic beta-cell function.
  • Increased miR-199 expression is observed in diabetic conditions.
  • Understanding miR-199 regulation in beta cells is crucial for diabetes research.

Purpose of the Study:

  • To investigate the regulatory mechanisms of miR-199 expression in pancreatic beta cells.
  • To assess the impact of glucose and calcium signaling on miR-199 precursor and mature forms.
  • To elucidate the role of glucose metabolism and calcium influx in miR-199 regulation.

Main Methods:

  • Quantitative analysis of miR-199 precursor (primiR-199a1, primiR-199a2, primiR-199b) and mature (miR-199-3p, miR-199-5p) expression.
  • Promoter transcriptional activity assays in mouse islets and MIN6 insulinoma cells.
  • Stimulation with varying glucose concentrations, KCl, tolbutamide, nifedipine, and diazoxide.

Main Results:

  • Glucose significantly up-regulates primiR-199a1 and primiR-199a2 mRNA levels in beta cells.
  • Calcium influx, stimulated by KCl, enhances primiR-199a2 expression and promoter activity.
  • Glucose metabolism and calcium signaling are key regulators of primiR-199a2, but not primiR-199a1.

Conclusions:

  • Glucose acutely increases miR-199 family expression in pancreatic beta cells.
  • The study identifies glucose metabolism and calcium influx as critical regulators of miR-199a2 expression.
  • Findings provide insights into the molecular mechanisms underlying miR-199 dysregulation in diabetes.
Keywords:
glucose metabolismislet functionmiR-199microRNA (miRNA)microRNA expressionpancreaspancreatic isletβ-cell

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