Downregulation of cyclin-dependent kinase inhibitor; p57kip2, is involved in the cell cycle progression of vascular smooth muscle cells

Noritsugu Nakano, Kazushi Urasawa, Yasushi Takagi, Takahiko Saito, Satoshi Kaneta, Susumu Ishikawa, Hideaki Higashi, Hiroyuki Tsutsui, Masanori Hatakeyama, Akira Kitabatake

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)

Abstract

Immature vascular smooth muscle cells (VSMCs) proliferate responding to extrinsic mitogens and accumulate in neointima after arterial injuries. Cell proliferation is positively regulated by cyclin/cyclin-dependent kinase (CDK) complex and negatively controlled by CDK inhibitors; CKIs such as p27 kip1 and p57kip2. In this study, embryonic rat thoracic aorta VSMCs; A10 were G0/G1 arrested by serum starvation, re-stimulated with serum, and harvested every four hours. Both CKIs co-expressed in quiescent VSMCs and rapidly diminished by stimulation. Protein level of p27kip1 was regulated by both transcription and post-transcription, but that of p57 kip2 was mainly by post-transcription. Supplemental overexpression of p57kip2 inhibited the activations of G1 cyclin/CDKs and subsequent hyperphosphorylations of all three retinoblastoma pocket proteins as well as G1/S transition of cell cycle. Our findings suggest that the downregulations of not only p27kip1, but also p57kip2 responding to mitogenic stimulation, play key roles in the cell cycle progression of VSMCs.

Original languageEnglish
Pages (from-to)1661-1667
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume338
Issue number3
DOIs
Publication statusPublished - Dec 23 2005
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Fingerprint Dive into the research topics of 'Downregulation of cyclin-dependent kinase inhibitor; p57<sup>kip2</sup>, is involved in the cell cycle progression of vascular smooth muscle cells'. Together they form a unique fingerprint.

Cite this