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Your search keyword '"Delafontaine, Patrice"' showing total 6 results
Start Over Author "Delafontaine, Patrice" Journal journal of molecular and cellular cardiology
6 results on '"Delafontaine, Patrice"'

2. β2 adrenergic activation induces the expression of IL-18 binding protein, a potent inhibitor of isoproterenol induced cardiomyocyte hypertrophy in vitro and myocardial hypertrophy in vivo

Author

Murray, David R., primary, Mummidi, Srinivas, additional, Valente, Anthony J., additional, Yoshida, Tadashi, additional, Somanna, Naveen K., additional, Delafontaine, Patrice, additional, Dinarello, Charles A., additional, and Chandrasekar, Bysani, additional

Published
2012
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6. EMMPRIN activates multiple transcription factors in cardiomyocytes, and induces interleukin-18 expression via Rac1-dependent PI3K/Akt/IKK/NF-kappaB andMKK7/JNK/AP-1 signaling.

Author

Venkatesan B, Valente AJ, Prabhu SD, Shanmugam P, Delafontaine P, and Chandrasekar B

Subjects
Animals, Basigin genetics, Cells, Cultured, Enzyme-Linked Immunosorbent Assay, MAP Kinase Kinase 7 metabolism, Male, Mice, Mice, Inbred C57BL, Myocytes, Cardiac drug effects, Phosphatidylinositol 3-Kinases metabolism, rac1 GTP-Binding Protein, Basigin metabolism, I-kappa B Kinase metabolism, Interleukin-18 genetics, Myocytes, Cardiac metabolism, NF-kappa B metabolism, Neuropeptides metabolism, Proto-Oncogene Proteins c-akt metabolism, Transcription Factor AP-1 metabolism, rac GTP-Binding Proteins metabolism
Abstract

The transmembrane glycoprotein extracellular matrix metalloproteinase inducer (EMMPRIN), and the pleiotropic proinflammatory cytokine interleukin (IL)-18, play critical roles in myocardial remodeling, by inducing matrix degrading metalloproteinases (MMPs). Previously we showed that IL-18 induces EMMPRIN expression in cardiomyocytes via MyD88/IRAK4/TRAF6/JNK-dependent Sp1 activation. Here in reciprocal studies we demonstrate that EMMPRIN is a potent inducer of IL-18 transcription, protein expression and protein secretion in primary mouse cardiomyocytes. We show for the first time that EMMPRIN stimulates the activation of NF-kappaB, AP-1, CREB, and ATF-2 in cardiomyocytes, and induces IL-18 expression via Rac1-dependent PI3K/Akt/IKK/NF-kappaB and MKK7/JNK/AP-1 signaling. Moreover, EMMPRIN induces robust time-dependent induction of various MMP mRNAs. EMMPRIN also induces the mRNA of TIMPs 1 and 3, but in a delayed fashion. These results suggest that IL-18-induced EMMPRIN expression may favor net MMP expression and ECM destruction, and thus identify both as potential therapeutic targets in countering adverse myocardial remodeling., (Copyright 2010 Elsevier Ltd. All rights reserved.)

Published
2010
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