PKGIα inhibits the proliferation of cerebral arterial smooth muscle cell induced by oxyhemoglobin after subarachnoid hemorrhage

Acta Neurochir Suppl. 2011;110(Pt 1):167-71. doi: 10.1007/978-3-7091-0353-1_29.

Abstract

The purpose of the present study was to observe the proliferation of cerebral arterial smooth muscle cell (CASMC) induced by oxyhemoglobin (Oxyhb) and interfered by Adenovirus-mediate-PKGI (Ad-PKGI), and to investigate the potential regulative role of the PKGI gene in the molecule mechanism of cerebral vasospasm (CVS) after Subarachnoid hemorrhage (SAH). Tissue-sticking method was used for primary cultured rat CASMCs. Semi-quantitative reverse transcription and polymerase chain reaction (RT-PCR) and western blot were used to examine the PKGI mRNA and protein expressions after CASMC were transfected by Ad-PKG. The proliferation of CASMCs was determined by MTT assay and 3H-TdR incorporation. Ad-PKGI could be transfected into CASMCS and highly express. Oxyhemoglobin could stimulate the proliferation of CASMC; the value of 3H-TdR incorporation and the absorbance value of MTT increased and could block up after CASMC was transfected by Ad-PKG. The results suggested that the PKG signaling pathway might play an important role in CVS after SAH, and the PKG gene might be a target point of gene therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Cell Count
  • Cell Proliferation / drug effects*
  • Cells, Cultured
  • Cerebral Arteries / anatomy & histology*
  • Cyclic GMP-Dependent Protein Kinase Type I
  • Cyclic GMP-Dependent Protein Kinases / genetics
  • Cyclic GMP-Dependent Protein Kinases / metabolism*
  • Enzyme Inhibitors / pharmacology
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / genetics
  • Muscle Cells / drug effects*
  • Muscle, Smooth / cytology*
  • Oxyhemoglobins / pharmacology*
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Tetrazolium Salts
  • Thiazoles
  • Transfection / methods

Substances

  • Enzyme Inhibitors
  • Oxyhemoglobins
  • RNA, Messenger
  • Tetrazolium Salts
  • Thiazoles
  • Cyclic GMP-Dependent Protein Kinase Type I
  • Cyclic GMP-Dependent Protein Kinases
  • thiazolyl blue