N-acetyl-seryl-aspartyl-lysyl-proline mediates the anti-fibrotic properties of captopril in unilateral ureteric obstructed BALB/C mice

Nephrology (Carlton). 2018 Apr;23(4):297-307. doi: 10.1111/nep.13000.

Abstract

Aim: Angiotensin-converting enzyme inhibitors (ACEi) are widely used to deter the progression of chronic kidney disease (CKD). Besides controlling hypertension and reduction of intra-glomerular pressure, ACEi appear to have anti-fibrotic effects in the renal cortex. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), an endogenous tetrapeptide that is degraded by ACE, has also been shown to ameliorate the pro-fibrotic phenotype displayed in CKD in our recent study. Whether the anti-fibrotic properties of ACEi are mediated by Ac-SDKP has not been fully investigated.

Methods: To delineate the role of Ac-SDKP in ACE blockade, 12-week-old male BALB/c mice underwent sham operation or unilateral ureteric obstruction (UUO). UUO mice were subjected to: (i) vehicle; (ii) captopril or (iii) captopril in conjunction with S17092, a prolyl oligopeptidase inhibitor. After 7 days, mice were sacrificed and kidneys harvested for analyses.

Results: After UUO, there were heightened expressions of collagen I, collagen III, fibronectin and α-SMA associated with significant levels of tubulointerstitial injury on histological examination. Furthermore, p44/42 mitogen-activated protein kinase (MAPK) and transforming growth factor beta 1(TGF-β1) signalling were upregulated. These were significantly ameliorated by captopril treatment alone but unaffected by co-administration of captopril with S17092. Captopril treatment had resulted in elevated urinary Ac-SDKP levels, an effect that was eliminated by the co-administration with S17092.

Conclusion: This study allowed the investigation of the renoprotective property of ACEi in the absence of Ac-SDKP and proved conclusively that Ac-SDKP is the prime anti-fibrotic mediator of captopril, acting via p44/42 MAPK and TGF-β1 signalling pathways. Future research to expand CKD armamentarium should explore the utility of augmenting Ac-SDKP levels.

Keywords: Anti-fibrotic; N-acetyl-seryl-aspartyl-lysyl-proline; chronic kidney disease; renoprotection; unilateral ureteric obstruction.

MeSH terms

  • Angiotensin-Converting Enzyme Inhibitors / pharmacology*
  • Animals
  • Captopril / pharmacology*
  • Disease Models, Animal
  • Extracellular Matrix Proteins / metabolism
  • Fibrosis
  • Indoles / pharmacology
  • Kidney / drug effects*
  • Kidney / metabolism
  • Kidney / pathology
  • Kidney Diseases / etiology
  • Kidney Diseases / metabolism
  • Kidney Diseases / pathology
  • Kidney Diseases / prevention & control*
  • Male
  • Mice, Inbred BALB C
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinase 3 / metabolism
  • Oligopeptides / metabolism*
  • Peptidyl-Dipeptidase A / metabolism
  • Prolyl Oligopeptidases
  • Serine Endopeptidases / metabolism
  • Serine Proteinase Inhibitors
  • Signal Transduction / drug effects
  • Thiazolidines / pharmacology
  • Transforming Growth Factor beta1 / metabolism
  • Ureteral Obstruction / complications
  • Ureteral Obstruction / drug therapy*
  • Ureteral Obstruction / metabolism
  • Ureteral Obstruction / pathology

Substances

  • Angiotensin-Converting Enzyme Inhibitors
  • Extracellular Matrix Proteins
  • Indoles
  • Oligopeptides
  • S 17092-1
  • Serine Proteinase Inhibitors
  • Tgfb1 protein, mouse
  • Thiazolidines
  • Transforming Growth Factor beta1
  • Captopril
  • Mapk1 protein, mouse
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • Peptidyl-Dipeptidase A
  • Serine Endopeptidases
  • Prolyl Oligopeptidases
  • goralatide