Lipopolysaccharide upregulates uPA, MMP-2 and MMP-9 via ERK1/2 signaling in H9c2 cardiomyoblast cells

ASIA unversity > 醫學暨健康學院 > 食品營養與保健生技學系 > 期刊論文 > Item 310904400/8423

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Title:	Lipopolysaccharide upregulates uPA, MMP-2 and MMP-9 via ERK1/2 signaling in H9c2 cardiomyoblast cells
Authors:	Cheng, YC (Cheng, Yi-Chang);Chen, LM (Chen, Li-Mien);Chang, MH (Chang, Mu-Hsin);Chen, WK (Chen, Wei-Kung);Tsai, FJ (Tsai, Fuu-Jen);Tsai, CH (Tsai, Chang-Hai);Lai, TY (Lai, Tung-Yuan);Kuo, WW (Kuo, Wei-Wen);Huang, CY (Huang, Chih-Yang);Liu, CJ (Liu, Chung-Jung)
Contributors:	保健系
Keywords:	Lipopolysaccharide;Myocardial cell;uPA;MMPs;ERK1/2 signaling pathway;TUMOR-NECROSIS-FACTOR;CHRONIC HEART-FAILURE;KINASE-DEPENDENT MECHANISM;CARDIAC MYOCYTE APOPTOSIS;ACTIVATED PROTEIN-KINASES;FACTOR-ALPHA;MATRIX METALLOPROTEINASES;MYOCARDIAL-INFARCTION;TISSUE INHIBITOR;DILATED CARDIOMYOPATHY
Date:	2009-05
Issue Date:	2010-03-26 02:46:36 (UTC+0)
Publisher:	Asia University
Abstract:	Upregulation of urokinase plasminogen activator (uPA), tissue plasminogen activator (tPA), and matrix metallopeptidases (MMPs) is associated with the development of myocardial infarction (MI), dilated cardiomyopathy, cardiac fibrosis, and heart failure (HF). Evidences suggest that lipopolysaccharide (LPS) participates in the inflammatory response in the cardiovascular system; however, it is unknown if LPS is sufficient to upregulate expressions and/or activity of uPA, tPA, MMP-2, and MMP-9 in myocardial cells. In this study, we treated H9c2 cardiomyoblasts with LPS to explore whether LPS upregulates uPA, tPA, MMP-2, and MMP-9, and further to identify the precise molecular and cellular mechanisms behind this upregulatory responses. Here, we show that LPS challenge increased the protein levels of uPA, MMP-2 and MMP-9, and induced the activity of MMP-2 and MMP-9 in H9c2 cardiomyoblasts. However, LPS showed no effects on the expression of tissue inhibitor of metalloproteinase-1, -2, -3, and -4 (TIMP-1, -2, -3, and -4). After administration of inhibitors including U0126 (ERK1/2 inhibitor), SB203580 (p38 MAPK inhibitor), SP600125 (JNK1/2 inhibitor), CsA (calcineurin inhibitor), and QNZ (NF kappa B inhibitor), the LPS-upregulated expression and/or activity of uPA, MMP-2, and MMP-9 in H9c2 cardiomyoblasts are markedly inhibited only by ERK1/2 inhibitors, U0126. Collectively, these results suggest that LPS upregulates the expression and/or activity of uPA, MMP-2, and MMP-9 through ERK1/2 signaling pathway in H9c2 cardiomyoblasts. Our findings further provide a link between the LPS-induced cardiac dysfunction and the ERK1/2 signaling pathway that mediates the upregulation of uPA, MMP-2 and MMP-9.
Relation:	MOLECULAR AND CELLULAR BIOCHEMISTRY 325 (1-2): 15-23
Appears in Collections:	[食品營養與保健生技學系] 期刊論文

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