[Evidence for retinoic acid modulating expression of cyclin-dependent kinase inhibitors in rat hepatic stellate cells]

Zhonghua Gan Zang Bing Za Zhi. 2001 Oct;9(5):306-8.
[Article in Chinese]

Abstract

Objective: To study the effects of retinoic acid on regulation of expressions of cyclin-dependent kinase inhibitors, i.e. p16, p21 and p27 in cultured rat hepatic stellate cells.

Methods: Stellate cells were isolated from healthy rat livers and cultured. After stimulated with 1 ng/ml transforming growth factor beta 1, subcultured hepatic stellate cells were treated with or without 1 nmol/ml retinoic acid. MTT assay, immunocytochemistry for p16, p21, p27 and alpha-smooth muscle actin protein, in situ hybridization for retinoic acid receptor beta 2 and p16, p21 and p27 mRNA and quantitative image analysis (partially) were performed.

Results: Retinoic acid markedly inhibited hepatic stellate cells proliferation (41.50%, P<0.05), decreased the protein level of alpha-smooth muscle actin (55.09%, P<0.05), and induced hepatic stellate cells to express retinoic acid receptor beta 2 mRNA. In addition, retinoic acid increased the protein level of p16 (218.75%, P <0.05) and induced p21 protein expression; meanwhile, p27 was undetectable by immunocytochemistry in both control and retinoic acid-treated hepatic stellate cells. However, retinoic acid had no influence on the mRNA level of p16, p21 or p27 as determined by in situ hybridization.

Conclusions: Up-regulation of p16 and p21 on post-transcriptional level may contribute, in part, to retinoic acid inhibition of transforming growth factor beta 1-initiated rat hepatic stellate cells activation in vitro.

Publication types

  • English Abstract

MeSH terms

  • Animals
  • Cell Cycle Proteins / biosynthesis
  • Cell Cycle Proteins / genetics
  • Cyclin-Dependent Kinase Inhibitor p16 / biosynthesis
  • Cyclin-Dependent Kinase Inhibitor p16 / genetics
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclin-Dependent Kinase Inhibitor p27
  • Cyclin-Dependent Kinases / antagonists & inhibitors*
  • Cyclins / biosynthesis
  • Cyclins / genetics
  • In Vitro Techniques
  • Liver / cytology
  • Liver / drug effects*
  • Liver / metabolism
  • Male
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / drug effects
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Retinoic Acid / biosynthesis
  • Receptors, Retinoic Acid / genetics
  • Transcription, Genetic / drug effects*
  • Transforming Growth Factor beta / antagonists & inhibitors
  • Transforming Growth Factor beta1
  • Tretinoin / pharmacology*
  • Tumor Suppressor Proteins / biosynthesis
  • Tumor Suppressor Proteins / genetics
  • Up-Regulation

Substances

  • Cdkn1a protein, rat
  • Cdkn1b protein, rat
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p16
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • RNA, Messenger
  • Receptors, Retinoic Acid
  • Tgfb1 protein, rat
  • Transforming Growth Factor beta
  • Transforming Growth Factor beta1
  • Tumor Suppressor Proteins
  • retinoic acid receptor beta
  • Cyclin-Dependent Kinase Inhibitor p27
  • Tretinoin
  • Cyclin-Dependent Kinases