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 language | English |
|---|---|
| Pages (from-to) | 1661-1667 |
| Number of pages | 7 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 338 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Dec 23 2005 |
| Externally published | Yes |
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All Science Journal Classification (ASJC) codes
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology
Cite this
Downregulation of cyclin-dependent kinase inhibitor; p57kip2, is involved in the cell cycle progression of vascular smooth muscle cells. / Nakano, Noritsugu; Urasawa, Kazushi; Takagi, Yasushi; Saito, Takahiko; Kaneta, Satoshi; Ishikawa, Susumu; Higashi, Hideaki; Tsutsui, Hiroyuki; Hatakeyama, Masanori; Kitabatake, Akira.
In: Biochemical and Biophysical Research Communications, Vol. 338, No. 3, 23.12.2005, p. 1661-1667.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Downregulation of cyclin-dependent kinase inhibitor; p57kip2, is involved in the cell cycle progression of vascular smooth muscle cells
AU - Nakano, Noritsugu
AU - Urasawa, Kazushi
AU - Takagi, Yasushi
AU - Saito, Takahiko
AU - Kaneta, Satoshi
AU - Ishikawa, Susumu
AU - Higashi, Hideaki
AU - Tsutsui, Hiroyuki
AU - Hatakeyama, Masanori
AU - Kitabatake, Akira
PY - 2005/12/23
Y1 - 2005/12/23
N2 - 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.
AB - 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=27744443696&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2005.10.093
DO - 10.1016/j.bbrc.2005.10.093
M3 - Article
VL - 338
SP - 1661
EP - 1667
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 3
ER -