Inhibitory role of magnolol on proliferative capacity and matrix metalloproteinase-9 expression in TNF-α-induced vascular smooth muscle cells

Hong Man Kim, Sung Jin Bae, Dong Wook Kim, Bo Kyung Kim, Soo Bok Lee, Ung Soo Lee, Cheorl Ho Kim, Sung Kwon Moon

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Magnolol, an active component extracted from Magnolia officinalis, has been reported to inhibit the development of atherosclerotic disease. However, it is not known whether magnolol exerts similar cardioprotective effects in cells treated with TNF-α. In the present study, magnolol treatment was found to show potent inhibitory effects on cell proliferation in cultured VSMC in the presence of TNF-α. These inhibitory effects were associated with reduced extracellular signal-regulated kinase (ERK) 1/2 activity and G1 cell cycle arrest. Magnolol treatment strongly induced the expression of p21WAF1, but resulted in a decrease in cyclin-dependent kinases (CDKs) and cyclins involved in G1 progression. In addition to G1 cell cycle arrest and growth inhibition in VSMC, magnolol also caused the strong inhibition of TNF-α-induced matrix metalloproteinase-9 (MMP-9) expression in a dose-dependent manner as determined by zymography and immunoblot. Moreover, magnolol treatment strongly decreased MMP-9 promoter activity in response to TNF-α. We further demonstrated that magnolol reduced the transcriptional activity of NF-κB and activation protein-1 (AP-1), two important nuclear transcription factors that are involved in MMP-9 expression. Collectively, these results show that magnolol inhibits cell proliferation, G1 to S phase cell cycle progress and MMP-9 expression through the transcription factors NF-κB and AP-1 in TNF-α-induced VSMC. The findings of the present study reveal a potential mechanism that explains the anti-atherogenic activity of magnolol.

Original languageEnglish
Pages (from-to)1083-1091
Number of pages9
JournalInternational Immunopharmacology
Volume7
Issue number8
DOIs
Publication statusPublished - 2007 Aug 1

Fingerprint

Matrix Metalloproteinase 9
Vascular Smooth Muscle
Smooth Muscle Myocytes
G1 Phase Cell Cycle Checkpoints
Transcription Factors
Magnolia
Cell Proliferation
magnolol
Cyclins
Mitogen-Activated Protein Kinase 3
Cyclin-Dependent Kinases
Mitogen-Activated Protein Kinase 1
S Phase
Cell Cycle
Growth

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Pharmacology

Cite this

Kim, Hong Man ; Bae, Sung Jin ; Kim, Dong Wook ; Kim, Bo Kyung ; Lee, Soo Bok ; Lee, Ung Soo ; Kim, Cheorl Ho ; Moon, Sung Kwon. / Inhibitory role of magnolol on proliferative capacity and matrix metalloproteinase-9 expression in TNF-α-induced vascular smooth muscle cells. In: International Immunopharmacology. 2007 ; Vol. 7, No. 8. pp. 1083-1091.
@article{beb4b705b1824ab2b9df3d0704a32e8e,
title = "Inhibitory role of magnolol on proliferative capacity and matrix metalloproteinase-9 expression in TNF-α-induced vascular smooth muscle cells",
abstract = "Magnolol, an active component extracted from Magnolia officinalis, has been reported to inhibit the development of atherosclerotic disease. However, it is not known whether magnolol exerts similar cardioprotective effects in cells treated with TNF-α. In the present study, magnolol treatment was found to show potent inhibitory effects on cell proliferation in cultured VSMC in the presence of TNF-α. These inhibitory effects were associated with reduced extracellular signal-regulated kinase (ERK) 1/2 activity and G1 cell cycle arrest. Magnolol treatment strongly induced the expression of p21WAF1, but resulted in a decrease in cyclin-dependent kinases (CDKs) and cyclins involved in G1 progression. In addition to G1 cell cycle arrest and growth inhibition in VSMC, magnolol also caused the strong inhibition of TNF-α-induced matrix metalloproteinase-9 (MMP-9) expression in a dose-dependent manner as determined by zymography and immunoblot. Moreover, magnolol treatment strongly decreased MMP-9 promoter activity in response to TNF-α. We further demonstrated that magnolol reduced the transcriptional activity of NF-κB and activation protein-1 (AP-1), two important nuclear transcription factors that are involved in MMP-9 expression. Collectively, these results show that magnolol inhibits cell proliferation, G1 to S phase cell cycle progress and MMP-9 expression through the transcription factors NF-κB and AP-1 in TNF-α-induced VSMC. The findings of the present study reveal a potential mechanism that explains the anti-atherogenic activity of magnolol.",
author = "Kim, {Hong Man} and Bae, {Sung Jin} and Kim, {Dong Wook} and Kim, {Bo Kyung} and Lee, {Soo Bok} and Lee, {Ung Soo} and Kim, {Cheorl Ho} and Moon, {Sung Kwon}",
year = "2007",
month = "8",
day = "1",
doi = "10.1016/j.intimp.2007.04.004",
language = "English",
volume = "7",
pages = "1083--1091",
journal = "International Immunopharmacology",
issn = "1567-5769",
publisher = "Elsevier",
number = "8",

}

Inhibitory role of magnolol on proliferative capacity and matrix metalloproteinase-9 expression in TNF-α-induced vascular smooth muscle cells. / Kim, Hong Man; Bae, Sung Jin; Kim, Dong Wook; Kim, Bo Kyung; Lee, Soo Bok; Lee, Ung Soo; Kim, Cheorl Ho; Moon, Sung Kwon.

In: International Immunopharmacology, Vol. 7, No. 8, 01.08.2007, p. 1083-1091.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Inhibitory role of magnolol on proliferative capacity and matrix metalloproteinase-9 expression in TNF-α-induced vascular smooth muscle cells

AU - Kim, Hong Man

AU - Bae, Sung Jin

AU - Kim, Dong Wook

AU - Kim, Bo Kyung

AU - Lee, Soo Bok

AU - Lee, Ung Soo

AU - Kim, Cheorl Ho

AU - Moon, Sung Kwon

PY - 2007/8/1

Y1 - 2007/8/1

N2 - Magnolol, an active component extracted from Magnolia officinalis, has been reported to inhibit the development of atherosclerotic disease. However, it is not known whether magnolol exerts similar cardioprotective effects in cells treated with TNF-α. In the present study, magnolol treatment was found to show potent inhibitory effects on cell proliferation in cultured VSMC in the presence of TNF-α. These inhibitory effects were associated with reduced extracellular signal-regulated kinase (ERK) 1/2 activity and G1 cell cycle arrest. Magnolol treatment strongly induced the expression of p21WAF1, but resulted in a decrease in cyclin-dependent kinases (CDKs) and cyclins involved in G1 progression. In addition to G1 cell cycle arrest and growth inhibition in VSMC, magnolol also caused the strong inhibition of TNF-α-induced matrix metalloproteinase-9 (MMP-9) expression in a dose-dependent manner as determined by zymography and immunoblot. Moreover, magnolol treatment strongly decreased MMP-9 promoter activity in response to TNF-α. We further demonstrated that magnolol reduced the transcriptional activity of NF-κB and activation protein-1 (AP-1), two important nuclear transcription factors that are involved in MMP-9 expression. Collectively, these results show that magnolol inhibits cell proliferation, G1 to S phase cell cycle progress and MMP-9 expression through the transcription factors NF-κB and AP-1 in TNF-α-induced VSMC. The findings of the present study reveal a potential mechanism that explains the anti-atherogenic activity of magnolol.

AB - Magnolol, an active component extracted from Magnolia officinalis, has been reported to inhibit the development of atherosclerotic disease. However, it is not known whether magnolol exerts similar cardioprotective effects in cells treated with TNF-α. In the present study, magnolol treatment was found to show potent inhibitory effects on cell proliferation in cultured VSMC in the presence of TNF-α. These inhibitory effects were associated with reduced extracellular signal-regulated kinase (ERK) 1/2 activity and G1 cell cycle arrest. Magnolol treatment strongly induced the expression of p21WAF1, but resulted in a decrease in cyclin-dependent kinases (CDKs) and cyclins involved in G1 progression. In addition to G1 cell cycle arrest and growth inhibition in VSMC, magnolol also caused the strong inhibition of TNF-α-induced matrix metalloproteinase-9 (MMP-9) expression in a dose-dependent manner as determined by zymography and immunoblot. Moreover, magnolol treatment strongly decreased MMP-9 promoter activity in response to TNF-α. We further demonstrated that magnolol reduced the transcriptional activity of NF-κB and activation protein-1 (AP-1), two important nuclear transcription factors that are involved in MMP-9 expression. Collectively, these results show that magnolol inhibits cell proliferation, G1 to S phase cell cycle progress and MMP-9 expression through the transcription factors NF-κB and AP-1 in TNF-α-induced VSMC. The findings of the present study reveal a potential mechanism that explains the anti-atherogenic activity of magnolol.

UR - http://www.scopus.com/inward/record.url?scp=34250377341&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34250377341&partnerID=8YFLogxK

U2 - 10.1016/j.intimp.2007.04.004

DO - 10.1016/j.intimp.2007.04.004

M3 - Article

C2 - 17570325

AN - SCOPUS:34250377341

VL - 7

SP - 1083

EP - 1091

JO - International Immunopharmacology

JF - International Immunopharmacology

SN - 1567-5769

IS - 8

ER -