title: [The role of cyclin-dependent kinase inhibitors in hyperplasia and hypertrophy of vascular smooth muscle cells].
abstract: OBJECTIVE
  To investigate the role p27, p21, and p57, different cyclin-dependent kinase inhibitors (CKIs), play in the hyperplasia and hypertrophy of vascular smooth muscle cells (VSMCs) stimulated with platelet-derived growth factor (PDGF-BB) and angiotensin II (Ang II).
  
  
  METHODS
  VSMCs from rat aorta were cultured. PDGF-BB and Ang II were added into the serum-free media at the concentrations of 10 - 6 M and 20 ng/ml respectively. VSMCs were harvested after 6h, 12h, and 24 h or stimulation. The protein levels of p27, p21 and p57 in VSMCs were examined with Western blot analysis.
  
  
  RESULTS
  The protein levels of p27, p21, and p57 in the Ang II-stimulated VSMCs were similar to those in the quiescent cells (P > 0.05). The protein levels of p21 and p57 in the PDGF-BB-stimulated VSMCs increased along with the time course of stimulation, the former being at its peak value at the 24th hour, and were significantly higher than those in Ang II-stimulated VSMCs. However, the p57 protein level was high in the quiescent cells. A remarkable decrease of the p57 protein level was found in the PDGF-BB-stimulated VSMCs (P < 0.01).
  
  
  CONCLUSIONS
  p27, p21, and p57 proteins play important roles in regulating hyperplasia and hypertrophy of VSMC. P21 and p57 prevent the overplasia of VSMCs. P27 is the most important regulator of hyperplasia and hypertrophy of VSMC stimulated by PDGF and Ang II.
authors.affiliation: Department of Cardiology, Nanfang Hospital, The First Military Medical University, Guangzhou 510515, China.
authors.forename: D
authors.initials: D
authors.lastname: Xu
authors.forename: M
authors.initials: M
authors.lastname: Wang
authors.forename: Y
authors.initials: Y
authors.lastname: Liu
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D000077214:Becaplermin; D018797:Cell Cycle Proteins / Q000378:metabolism* / Q000502:physiology; D050759:Cyclin-Dependent Kinase Inhibitor p21; D050760:Cyclin-Dependent Kinase Inhibitor p27; D050761:Cyclin-Dependent Kinase Inhibitor p57; D016213:Cyclins / Q000378:metabolism* / Q000502:physiology; D004195:Disease Models, Animal; D015870:Gene Expression / Q000187:drug effects; D006965:Hyperplasia / Q000378:metabolism; D006984:Hypertrophy / Q000378:metabolism; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology*; D009687:Nuclear Proteins / Q000378:metabolism* / Q000502:physiology; D010982:Platelet-Derived Growth Factor / Q000494:pharmacology; D020574:Proto-Oncogene Proteins c-sis; D051381:Rats; D017207:Rats, Sprague-Dawley; D025521:Tumor Suppressor Proteins / Q000378:metabolism* / Q000502:physiology
chemical_list: C493958:Cdkn1a protein, rat; C493962:Cdkn1b protein, rat; D018797:Cell Cycle Proteins; D050759:Cyclin-Dependent Kinase Inhibitor p21; D050761:Cyclin-Dependent Kinase Inhibitor p57; D016213:Cyclins; D009687:Nuclear Proteins; D010982:Platelet-Derived Growth Factor; D020574:Proto-Oncogene Proteins c-sis; D025521:Tumor Suppressor Proteins; D000804:Angiotensin II; D050760:Cyclin-Dependent Kinase Inhibitor p27; D000077214:Becaplermin