skip to main content
OSTI.GOV title logo U.S. Department of Energy
Office of Scientific and Technical Information

Title: Effects and underlying mechanisms of curcumin on the proliferation of vascular smooth muscle cells induced by Chol:M{beta}CD

Abstract

Proliferation of vascular smooth muscle cells (VSMCs) contributes to the development of various cardiovascular diseases. Curcumin, extracted from Curcumae longae, has been shown a variety of beneficial effects on human health, including anti-atherosclerosis by mechanisms poorly understood. In the present study, we attempted to investigate whether curcumin has any effect on VSMCs proliferation and the potential mechanisms involved. Our data showed curcumin concentration-dependently abrogated the proliferation of primary rat VSMCs induced by Chol:M{beta}CD. To explore the underlying cellular and molecular mechanisms, we found that curcumin was capable of restoring caveolin-1 expression which was reduced by Chol:M{beta}CD treatment. Moreover, curcumin abrogated the increment of phospho-ERK1/2 and nuclear accumulation of ERK1/2 in primary rat VSMCs induced by Chol:M{beta}CD, which led to a suppression of AP-1 promoter activity stimulated by Chol:M{beta}CD. In addition, curcumin was able to reverse cell cycle progression induced by Chol:M{beta}CD, which was further supported by its down-regulation of cyclinD1 and E2F promoter activities in the presence of Chol:M{beta}CD. Taking together, our data suggest curcumin inhibits Chol:M{beta}CD-induced VSMCs proliferation via restoring caveolin-1 expression that leads to the suppression of over-activated ERK signaling and causes cell cycle arrest at G1/S phase. These novel findings support the beneficial potential of curcumin inmore » cardiovascular disease.« less

Authors:
 [1]; ; ; ;  [2];  [1]
  1. Department of Pharmacology, School of Pharmaceutical Science, Central South University, Changsha 410078 (China)
  2. Division of Pharmacoproteomics, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001 (China)
Publication Date:
OSTI Identifier:
21255854
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 379; Journal Issue: 2; Other Information: DOI: 10.1016/j.bbrc.2008.12.038; PII: S0006-291X(08)02424-8; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ARTERIOSCLEROSIS; CELL CYCLE; CELL PROLIFERATION; CURCUMIN; ENZYME INHIBITORS; GENE REGULATION; MUSCLES; PROMOTERS; PUBLIC HEALTH; RATS

Citation Formats

Li, Qin, Division of Pharmacoproteomics, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001, Yunbo, Yang, Qinhui, Tuo, Bingyang, Zhu, Linxi, Chen, Zhang Liang, Duanfang, Liao, and Division of Pharmacoproteomics, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001. Effects and underlying mechanisms of curcumin on the proliferation of vascular smooth muscle cells induced by Chol:M{beta}CD. United States: N. p., 2009. Web. doi:10.1016/j.bbrc.2008.12.038.
Li, Qin, Division of Pharmacoproteomics, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001, Yunbo, Yang, Qinhui, Tuo, Bingyang, Zhu, Linxi, Chen, Zhang Liang, Duanfang, Liao, & Division of Pharmacoproteomics, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001. Effects and underlying mechanisms of curcumin on the proliferation of vascular smooth muscle cells induced by Chol:M{beta}CD. United States. https://doi.org/10.1016/j.bbrc.2008.12.038
Li, Qin, Division of Pharmacoproteomics, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001, Yunbo, Yang, Qinhui, Tuo, Bingyang, Zhu, Linxi, Chen, Zhang Liang, Duanfang, Liao, and Division of Pharmacoproteomics, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001. 2009. "Effects and underlying mechanisms of curcumin on the proliferation of vascular smooth muscle cells induced by Chol:M{beta}CD". United States. https://doi.org/10.1016/j.bbrc.2008.12.038.
@article{osti_21255854,
title = {Effects and underlying mechanisms of curcumin on the proliferation of vascular smooth muscle cells induced by Chol:M{beta}CD},
author = {Li, Qin and Division of Pharmacoproteomics, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001 and Yunbo, Yang and Qinhui, Tuo and Bingyang, Zhu and Linxi, Chen and Zhang Liang and Duanfang, Liao and Division of Pharmacoproteomics, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001},
abstractNote = {Proliferation of vascular smooth muscle cells (VSMCs) contributes to the development of various cardiovascular diseases. Curcumin, extracted from Curcumae longae, has been shown a variety of beneficial effects on human health, including anti-atherosclerosis by mechanisms poorly understood. In the present study, we attempted to investigate whether curcumin has any effect on VSMCs proliferation and the potential mechanisms involved. Our data showed curcumin concentration-dependently abrogated the proliferation of primary rat VSMCs induced by Chol:M{beta}CD. To explore the underlying cellular and molecular mechanisms, we found that curcumin was capable of restoring caveolin-1 expression which was reduced by Chol:M{beta}CD treatment. Moreover, curcumin abrogated the increment of phospho-ERK1/2 and nuclear accumulation of ERK1/2 in primary rat VSMCs induced by Chol:M{beta}CD, which led to a suppression of AP-1 promoter activity stimulated by Chol:M{beta}CD. In addition, curcumin was able to reverse cell cycle progression induced by Chol:M{beta}CD, which was further supported by its down-regulation of cyclinD1 and E2F promoter activities in the presence of Chol:M{beta}CD. Taking together, our data suggest curcumin inhibits Chol:M{beta}CD-induced VSMCs proliferation via restoring caveolin-1 expression that leads to the suppression of over-activated ERK signaling and causes cell cycle arrest at G1/S phase. These novel findings support the beneficial potential of curcumin in cardiovascular disease.},
doi = {10.1016/j.bbrc.2008.12.038},
url = {https://www.osti.gov/biblio/21255854}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 2,
volume = 379,
place = {United States},
year = {Fri Feb 06 00:00:00 EST 2009},
month = {Fri Feb 06 00:00:00 EST 2009}
}