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

doi:10.1016/j.bbrc.2005.10.093

Downregulation of cyclin-dependent kinase inhibitor; p57^kip2, 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 journal › Article › peer-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 p57^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^kip1 was regulated by both transcription and post-transcription, but that of p57 ^kip2 was mainly by post-transcription. Supplemental overexpression of p57^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^kip1, but also p57^kip2 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	https://doi.org/10.1016/j.bbrc.2005.10.093
Publication status	Published - Dec 23 2005
Externally published	Yes

All Science Journal Classification (ASJC) codes

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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Nakano, N., Urasawa, K., Takagi, Y., Saito, T., Kaneta, S., Ishikawa, S., Higashi, H., Tsutsui, H., Hatakeyama, M., & Kitabatake, A. (2005). Downregulation of cyclin-dependent kinase inhibitor; p57^kip2, is involved in the cell cycle progression of vascular smooth muscle cells. Biochemical and Biophysical Research Communications, 338(3), 1661-1667. https://doi.org/10.1016/j.bbrc.2005.10.093

Downregulation of cyclin-dependent kinase inhibitor; p57^kip2, 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 › peer-review

Nakano, N, Urasawa, K, Takagi, Y, Saito, T, Kaneta, S, Ishikawa, S, Higashi, H, Tsutsui, H, Hatakeyama, M & Kitabatake, A 2005, 'Downregulation of cyclin-dependent kinase inhibitor; p57^kip2, is involved in the cell cycle progression of vascular smooth muscle cells', Biochemical and Biophysical Research Communications, vol. 338, no. 3, pp. 1661-1667. https://doi.org/10.1016/j.bbrc.2005.10.093

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^kip2, is involved in the cell cycle progression of vascular smooth muscle cells. In: Biochemical and Biophysical Research Communications. 2005 ; Vol. 338, No. 3. pp. 1661-1667.

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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.",

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AU - Kaneta, Satoshi

AU - Ishikawa, Susumu

AU - Higashi, Hideaki

AU - Tsutsui, Hiroyuki

AU - Hatakeyama, Masanori

AU - Kitabatake, Akira

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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.

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