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Short homologous peptides based on C-terminal sequences of fibrinogen β- and γ-chains (Haptides) affect

Maamoun Basheer1, Herzl Schwalb, Dan Gilon

  • 1Laboratory of Biotechnology and Radiobiology, Sharett Institute of Oncology, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.

Journal of Vascular Research
|May 1, 2010
PubMed

Insights

Haptides, peptides homologous to fibrinogen, impair heart function by inhibiting endothelial nitric oxide synthase (eNOS) and causing vasoconstriction. These effects were dose-dependent and reversible with NO donors.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Biology
  • Pharmacology

Background:

  • Haptides are cell-binding peptides homologous to fibrinogen C-termini.
  • Their cardiovascular effects are not well-understood.

Purpose of the Study:

  • To investigate the impact of Haptides on cardiovascular function.
  • To elucidate the mechanism of Haptide-induced cardiovascular effects.

Main Methods:

  • Isolated perfused rat heart and blood vessel assays.
  • Measurement of hemodynamic functions and eNOS activity.
  • Use of NO donor (sodium nitroprusside) and eNOS inhibitor (L-NAME).

Main Results:

  • Haptides dose-dependently decreased rat heart hemodynamic functions.
  • Haptides inhibited eNOS activity in myocardial homogenates and HUVEC.
  • Haptides caused vasoconstriction in intact aorta and mammary artery vessels.
  • NO donor reversed Haptide-induced inhibition; eNOS inhibitor did not augment effects.

Conclusions:

  • Haptides affect coronary endothelium by inhibiting eNOS activity.
  • This inhibition leads to vasoconstriction, ischemia, and impaired myocardial function.
  • Cardiovascular effects are linked to Haptide's amino acid composition and interaction with endothelium, not cardiomyocytes.

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