Effect of N-acetyl-seryl-aspartyl-lysyl-proline on DNA and collagen synthesis in rat cardiac fibroblasts

Hypertension. 2001 Mar;37(3):827-32. doi: 10.1161/01.hyp.37.3.827.

Abstract

N:-Acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a natural inhibitor of pluripotent hematopoietic stem cell entry into the S phase of the cell cycle and is normally present in human plasma. Ac-SDKP is exclusively hydrolyzed by ACE, and its plasma concentration is increased 5-fold after ACE inhibition in humans. We examined the effect of 0.05 to 100 nmol/L Ac-SDKP on 24-hour (3)H-thymidine incorporation (DNA synthesis) by cardiac fibroblasts both in the absence and presence of 5% FCS. Captopril (1 micromol/L) was added in all cases to prevent the degradation of Ac-SDKP. Treatment of cardiac fibroblasts with 5% FCS increased thymidine incorporation from a control value of 12 469+/-594 to 24 598+/-1051 cpm (P:<0.001). Cotreatment with 1 nmol/L Ac-SDKP reduced stimulation to control levels (10 373+/-200 cpm, P:<0.001). We measured hydroxyproline content and incorporation of (3)H-proline into collagenous fibroblast proteins and found that Ac-SDKP blocked endothelin-1 (10(-8) mol/L)-induced collagen synthesis in a biphasic and dose-dependent manner, causing inhibition at low doses, whereas high doses had little or no effect. It also blunted the activity of p44/p42 mitogen-activated protein kinase in a biphasic and dose-dependent manner in serum-stimulated fibroblasts, suggesting that the inhibitory effect of DNA and collagen synthesis may depend in part on blocking mitogen-activated protein kinase activity. Participation of p44/p42 in collagen synthesis was confirmed, because a specific inhibitor for p44/p42 activation (PD 98059, 25 micromol/L) was able to block endothelin-1-induced collagen synthesis, similar to the effect of Ac-SDKP. The fact that Ac-SDKP inhibits DNA and collagen synthesis in cardiac fibroblasts suggests that it may be an important endogenous regulator of fibroblast proliferation and collagen synthesis in the heart. Ac-SDKP may participate in the cardioprotective effect of ACE inhibitors by limiting fibroblast proliferation (and hence collagen production), and therefore it would reduce fibrosis in patients with hypertension.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Angiotensin II / physiology*
  • Angiotensin Receptor Antagonists
  • Angiotensin-Converting Enzyme Inhibitors / metabolism
  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use
  • Animals
  • Cell Division / drug effects
  • Cells, Cultured
  • Collagen / biosynthesis*
  • DNA / biosynthesis
  • Dose-Response Relationship, Drug
  • Endothelin-1 / antagonists & inhibitors
  • Enzyme Activation / drug effects
  • Enzyme Inhibitors / pharmacology
  • Fibrosis / drug therapy
  • Gene Expression Regulation / drug effects
  • Humans
  • Hypertension / drug therapy
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • Mitogen-Activated Protein Kinases / metabolism
  • Myocardium / metabolism*
  • Oligopeptides / blood
  • Oligopeptides / metabolism
  • Oligopeptides / pharmacology*
  • Peptidyl-Dipeptidase A / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Receptor, Angiotensin, Type 1
  • Receptor, Angiotensin, Type 2
  • Receptors, Angiotensin / metabolism
  • Renin-Angiotensin System

Substances

  • Angiotensin Receptor Antagonists
  • Angiotensin-Converting Enzyme Inhibitors
  • Endothelin-1
  • Enzyme Inhibitors
  • Oligopeptides
  • Receptor, Angiotensin, Type 1
  • Receptor, Angiotensin, Type 2
  • Receptors, Angiotensin
  • Angiotensin II
  • Collagen
  • DNA
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases
  • Peptidyl-Dipeptidase A
  • goralatide