Inhibition of the expression of TGF-β1 and CTGF in human mesangial cells by exendin-4, a glucagon-like peptide-1 receptor agonist

Cell Physiol Biochem. 2012;30(3):749-57. doi: 10.1159/000341454. Epub 2012 Aug 2.

Abstract

Background: Despite the presence of glucagon-like peptide-1 receptor (GLP-1R) in kidney tissues, its direct effect on diabetic nephropathy remains unclear. The transforming growth factor-β(1) (TGF-β(1)) and the connective tissue growth factor (CTGF) both induce extracellular matrix accumulation and persistent fibrosis in the glomerular mesangium of patients with diabetic nephropathy.

Objective: Herein, we demonstrate that a GLP-1R agonist, exendin-4, exerts renoprotective effects through its influence on TGF-β(1) and CTGF in human mesangial cells (HMCs), cultured in a high glucose medium.

Method: HMCs, cultured in a high glucose medium, were used for the current study. The direct effect of exendin-4 on TGF-β(1) and CTGF expression was confirmed in HMCs. MDL-12330A (a specific adenylate cyclase inhibitor) and PKI14-22 (a protein kinase A inhibitor) were used to examine the role of the cAMP signaling pathway in exendin's anti-fibrosis action.

Results: The findings showed that exendin-4 inhibited the proliferation of HMCs, and upregulated the expression of TGF-β(1) and CTGF, induced by high glucose. The effect of exendin-4 is largely dependent on the activation of adenylate cyclase.

Conclusion: This study provides new evidence that GLP-1 acts as an antifibrotic agent in HMCs.

MeSH terms

  • Adenylyl Cyclase Inhibitors
  • Adenylyl Cyclases / metabolism
  • Carrier Proteins / pharmacology
  • Cell Proliferation / drug effects
  • Cells, Cultured
  • Connective Tissue Growth Factor / genetics
  • Connective Tissue Growth Factor / metabolism*
  • Cyclic AMP / metabolism
  • Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Exenatide
  • Extracellular Matrix / metabolism
  • Glucagon-Like Peptide-1 Receptor
  • Glucose / pharmacology
  • Humans
  • Imines / pharmacology
  • Mesangial Cells / drug effects
  • Mesangial Cells / metabolism
  • Peptide Fragments / pharmacology
  • Peptides / pharmacology*
  • Receptors, Glucagon / agonists*
  • Receptors, Glucagon / metabolism
  • Signal Transduction / drug effects
  • Transforming Growth Factor beta1 / genetics
  • Transforming Growth Factor beta1 / metabolism*
  • Up-Regulation / drug effects
  • Venoms / pharmacology*

Substances

  • Adenylyl Cyclase Inhibitors
  • Carrier Proteins
  • GLP1R protein, human
  • Glucagon-Like Peptide-1 Receptor
  • Imines
  • Peptide Fragments
  • Peptides
  • Receptors, Glucagon
  • Transforming Growth Factor beta1
  • Venoms
  • myristoylated protein kinase A inhibitor amide 14-22
  • Connective Tissue Growth Factor
  • RMI 12330A
  • Exenatide
  • Cyclic AMP
  • Cyclic AMP-Dependent Protein Kinases
  • Adenylyl Cyclases
  • Glucose