Thrombin-induced mitogenesis in cultured aortic smooth muscle cells requires prolonged thrombin exposure

Am J Physiol. 1995 May;268(5 Pt 1):C1141-7. doi: 10.1152/ajpcell.1995.268.5.C1141.

Abstract

Thrombin has been implicated in vascular smooth muscle cell (VSMC) proliferation after vessel injury. Its proliferative effects, which are mediated via proteolytic activation of a receptor similar or identical to the cloned thrombin receptor (TR), have markedly delayed kinetics. The present study demonstrates that, despite rapid thrombin receptor activation and similar time to S phase entry compared with classic polypeptide growth factors, prolonged thrombin exposure is required to promote maximal VSMC mitogenesis. Flow cytometric analysis of thrombin-stimulated cells revealed that thrombin induced a progressive increase in the growth fraction over 3 days in culture, an effect that was blocked by hirudin even late after thrombin addition. Northern blot hybridization after thrombin stimulation demonstrated that thrombin upregulates TR mRNA expression within 6 h. These findings indicate that VSMC proliferate in response to prolonged thrombin exposure and suggest that the mitogenic delay may involve not only the thrombin-dependent synthesis and activation of newly made TR but also the progressive thrombin-dependent recruitment of cells into the growth fraction.

Publication types

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

MeSH terms

  • Animals
  • Aorta / cytology
  • Aorta / drug effects*
  • Base Sequence
  • Cells, Cultured
  • Cytosol / metabolism
  • Mitogens / pharmacology*
  • Molecular Probes / genetics
  • Molecular Sequence Data
  • Muscle, Smooth, Vascular / cytology
  • Muscle, Smooth, Vascular / drug effects*
  • RNA, Messenger / metabolism
  • Rats
  • Receptors, Thrombin / genetics
  • S Phase
  • Thrombin / pharmacology*
  • Time Factors

Substances

  • Mitogens
  • Molecular Probes
  • RNA, Messenger
  • Receptors, Thrombin
  • Thrombin