Progesterone-Induced migration inhibition in male rat aortic smooth muscle cells through the cSrc/AKT/ERK 2/p38 Pathway-Mediated Up-Regulation of p27

Hui Chen Wang, Wen Sen Lee

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Previously, we showed that progesterone (P4) inhibits proliferation and migration of rat aortic smooth musclecells (RASMCs). The P4-induced migration inhibition in RASMCs resulted from suppression of the Ras homolog gene family, member A (RhoA) activity mediated by cSrc activation. We also observed that P4 increased the formation of p27-RhoA complex in RASMCs. The aim of this study was to further study the involvement of p27 in P4-induced migration inhibition in RASMCs. Treatment with P4 (50 nM) increased the level of p27 protein in RASMCs. Knockdown of p27 abolished the P4-induced increases of the levels of p27 protein and decreases of cell migration in RASMCs. We conducted Western blot analyses and applied pharmacologic inhibitors to delineate the signaling pathway involved in the P4-induced p27 up-regulation and migration inhibition in RASMCs. Our data suggest that P4 increased the levels of p27 in RASMCs through activating the cSrc/AKT/ERK 2/p38 pathway mediated by non-genomic progesterone receptor. The findings of the present study highlight the molecular mechanisms underlying P4-induced migration inhibition in RASMCs.

Original languageEnglish
Pages (from-to)1428-1435
Number of pages8
JournalEndocrinology
Volume155
Issue number4
DOIs
Publication statusPublished - Apr 2014

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Smooth Muscle Myocytes
Progesterone
Up-Regulation
ras Genes
Inhibition (Psychology)
Progesterone Receptors
Cell Movement
Western Blotting
Proteins

ASJC Scopus subject areas

  • Endocrinology

Cite this

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title = "Progesterone-Induced migration inhibition in male rat aortic smooth muscle cells through the cSrc/AKT/ERK 2/p38 Pathway-Mediated Up-Regulation of p27",
abstract = "Previously, we showed that progesterone (P4) inhibits proliferation and migration of rat aortic smooth musclecells (RASMCs). The P4-induced migration inhibition in RASMCs resulted from suppression of the Ras homolog gene family, member A (RhoA) activity mediated by cSrc activation. We also observed that P4 increased the formation of p27-RhoA complex in RASMCs. The aim of this study was to further study the involvement of p27 in P4-induced migration inhibition in RASMCs. Treatment with P4 (50 nM) increased the level of p27 protein in RASMCs. Knockdown of p27 abolished the P4-induced increases of the levels of p27 protein and decreases of cell migration in RASMCs. We conducted Western blot analyses and applied pharmacologic inhibitors to delineate the signaling pathway involved in the P4-induced p27 up-regulation and migration inhibition in RASMCs. Our data suggest that P4 increased the levels of p27 in RASMCs through activating the cSrc/AKT/ERK 2/p38 pathway mediated by non-genomic progesterone receptor. The findings of the present study highlight the molecular mechanisms underlying P4-induced migration inhibition in RASMCs.",
author = "Wang, {Hui Chen} and Lee, {Wen Sen}",
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AU - Wang, Hui Chen

AU - Lee, Wen Sen

PY - 2014/4

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N2 - Previously, we showed that progesterone (P4) inhibits proliferation and migration of rat aortic smooth musclecells (RASMCs). The P4-induced migration inhibition in RASMCs resulted from suppression of the Ras homolog gene family, member A (RhoA) activity mediated by cSrc activation. We also observed that P4 increased the formation of p27-RhoA complex in RASMCs. The aim of this study was to further study the involvement of p27 in P4-induced migration inhibition in RASMCs. Treatment with P4 (50 nM) increased the level of p27 protein in RASMCs. Knockdown of p27 abolished the P4-induced increases of the levels of p27 protein and decreases of cell migration in RASMCs. We conducted Western blot analyses and applied pharmacologic inhibitors to delineate the signaling pathway involved in the P4-induced p27 up-regulation and migration inhibition in RASMCs. Our data suggest that P4 increased the levels of p27 in RASMCs through activating the cSrc/AKT/ERK 2/p38 pathway mediated by non-genomic progesterone receptor. The findings of the present study highlight the molecular mechanisms underlying P4-induced migration inhibition in RASMCs.

AB - Previously, we showed that progesterone (P4) inhibits proliferation and migration of rat aortic smooth musclecells (RASMCs). The P4-induced migration inhibition in RASMCs resulted from suppression of the Ras homolog gene family, member A (RhoA) activity mediated by cSrc activation. We also observed that P4 increased the formation of p27-RhoA complex in RASMCs. The aim of this study was to further study the involvement of p27 in P4-induced migration inhibition in RASMCs. Treatment with P4 (50 nM) increased the level of p27 protein in RASMCs. Knockdown of p27 abolished the P4-induced increases of the levels of p27 protein and decreases of cell migration in RASMCs. We conducted Western blot analyses and applied pharmacologic inhibitors to delineate the signaling pathway involved in the P4-induced p27 up-regulation and migration inhibition in RASMCs. Our data suggest that P4 increased the levels of p27 in RASMCs through activating the cSrc/AKT/ERK 2/p38 pathway mediated by non-genomic progesterone receptor. The findings of the present study highlight the molecular mechanisms underlying P4-induced migration inhibition in RASMCs.

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