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Title: Downregulation of cyclin-dependent kinase inhibitor; p57{sup kip2}, is involved in the cell cycle progression of vascular smooth muscle cells

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{sup kip1} and p57{sup kip2}. 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 p27{sup kip1} was regulated by both transcription and post-transcription, but that of p57{sup kip2} was mainly by post-transcription. Supplemental overexpression of p57{sup kip2} 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 p27{sup kip1}, but also p57{sup kip2} responding to mitogenic stimulation, play key roles in the cell cycle progression of VSMCs.

Authors:
 [1];  [2];  [2];  [2];  [2];  [3];  [3];  [2];  [3];  [2]
  1. Department of Cardiovascular Medicine, Graduate School of Medicine, Hokkaido University, Sapporo 060-8638 (Japan). E-mail: norida@med.hokudai.ac.jp
  2. Department of Cardiovascular Medicine, Graduate School of Medicine, Hokkaido University, Sapporo 060-8638 (Japan)
  3. Division of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815 (Japan)
Publication Date:
OSTI Identifier:
20793239
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 338; Journal Issue: 3; Other Information: DOI: 10.1016/j.bbrc.2005.10.093; PII: S0006-291X(05)02344-2; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; AORTA; CELL CYCLE; CELL PROLIFERATION; INJURIES; MITOGENS; MUSCLES; PROTEINS; RATS; STIMULATION; TRANSCRIPTION

Citation Formats

Nakano, Noritsugu, Urasawa, Kazushi, Takagi, Yasushi, Saito, Takahiko, Kaneta, Satoshi, Ishikawa, Susumu, Higashi, Hideaki, Tsutsui, Hiroyuki, Hatakeyama, Masanori, and Kitabatake, Akira. Downregulation of cyclin-dependent kinase inhibitor; p57{sup kip2}, is involved in the cell cycle progression of vascular smooth muscle cells. United States: N. p., 2005. Web. doi:10.1016/J.BBRC.2005.1.
Nakano, Noritsugu, Urasawa, Kazushi, Takagi, Yasushi, Saito, Takahiko, Kaneta, Satoshi, Ishikawa, Susumu, Higashi, Hideaki, Tsutsui, Hiroyuki, Hatakeyama, Masanori, & Kitabatake, Akira. Downregulation of cyclin-dependent kinase inhibitor; p57{sup kip2}, is involved in the cell cycle progression of vascular smooth muscle cells. United States. doi:10.1016/J.BBRC.2005.1.
Nakano, Noritsugu, Urasawa, Kazushi, Takagi, Yasushi, Saito, Takahiko, Kaneta, Satoshi, Ishikawa, Susumu, Higashi, Hideaki, Tsutsui, Hiroyuki, Hatakeyama, Masanori, and Kitabatake, Akira. Fri . "Downregulation of cyclin-dependent kinase inhibitor; p57{sup kip2}, is involved in the cell cycle progression of vascular smooth muscle cells". United States. doi:10.1016/J.BBRC.2005.1.
@article{osti_20793239,
title = {Downregulation of cyclin-dependent kinase inhibitor; p57{sup kip2}, is involved in the cell cycle progression of vascular smooth muscle cells},
author = {Nakano, Noritsugu and Urasawa, Kazushi and Takagi, Yasushi and Saito, Takahiko and Kaneta, Satoshi and Ishikawa, Susumu and Higashi, Hideaki and Tsutsui, Hiroyuki and Hatakeyama, Masanori and Kitabatake, Akira},
abstractNote = {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{sup kip1} and p57{sup kip2}. 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 p27{sup kip1} was regulated by both transcription and post-transcription, but that of p57{sup kip2} was mainly by post-transcription. Supplemental overexpression of p57{sup kip2} 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 p27{sup kip1}, but also p57{sup kip2} responding to mitogenic stimulation, play key roles in the cell cycle progression of VSMCs.},
doi = {10.1016/J.BBRC.2005.1},
journal = {Biochemical and Biophysical Research Communications},
number = 3,
volume = 338,
place = {United States},
year = {Fri Dec 23 00:00:00 EST 2005},
month = {Fri Dec 23 00:00:00 EST 2005}
}