p38 mitogen-activated protein kinase inhibition decreases TNFalpha secretion and protects against left ventricular remodeling in rats with myocardial ischemia

Inflammation

Volumn 31, Issue 2, 2008, Pages 65-73

  Yin, Huiqiu ^a   Zhang, Jidong ^a   Lin, Haiqing ^b   Wang, Rong ^a   Qiao, Yun ^a   Wang, Bo ^a   Liu, Fenye ^a  

^a SHANDONG UNIVERSITY   (China)

^b SHANDONG UNIVERSITY OF TRADITIONAL CHINESE MEDICINE   (China)

Author keywords

Inflammatory cytokine; Left ventricular remodeling; Myocardial fibrosis; Myocardial ischemia

Indexed keywords

4 (4 FLUOROPHENYL) 2 (4 METHYLSULFINYLPHENYL) 5 (4 PYRIDYL)IMIDAZOLE; ALPHA SMOOTH MUSCLE ACTIN; COLLAGEN TYPE 1; MITOGEN ACTIVATED PROTEIN KINASE P38; TUMOR NECROSIS FACTOR ALPHA;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; CORONARY ARTERY LIGATION; DRUG MECHANISM; ECHOCARDIOGRAPHY; ENZYME INHIBITION; HEART FUNCTION; HEART MUSCLE FIBROSIS; HEART MUSCLE ISCHEMIA; HEART VENTRICLE REMODELING; IMMUNOHISTOCHEMISTRY; NONHUMAN; RAT; TRANSMISSION ELECTRON MICROSCOPY; WESTERN BLOTTING;

ACTINS; ANIMALS; BLOTTING, WESTERN; COLLAGEN TYPE I; CORONARY VESSELS; DISEASE MODELS, ANIMAL; DOWN-REGULATION; ECHOCARDIOGRAPHY; FIBROSIS; IMIDAZOLES; IMMUNOHISTOCHEMISTRY; INJECTIONS, INTRAPERITONEAL; LIGATION; MICROSCOPY, ELECTRON, TRANSMISSION; MYOCARDIAL ISCHEMIA; MYOCARDIUM; P38 MITOGEN-ACTIVATED PROTEIN KINASES; PHOSPHORYLATION; PROTEIN KINASE INHIBITORS; PYRIDINES; RATS; RATS, WISTAR; SIGNAL TRANSDUCTION; TIME FACTORS; TUMOR NECROSIS FACTOR-ALPHA; VENTRICULAR FUNCTION, LEFT; VENTRICULAR REMODELING;

RATTUS;

EID: 40749144924     PISSN: 03603997     EISSN: None     Source Type: Journal    
DOI: 10.1007/s10753-007-9050-2     Document Type: Article

References (22)

1. Martine, R. M. 2006. Cardiac remodeling and inflammation. Arch. Cardiol. Mex. 76:S58-S66.
2. Manning, A. M., and R. J. Davis. 2003. Targeting JNK for therapeutic benefit: from junk to gold? Nat. Rev. Drug Discov. 2:554-565.
3. Karin, M., and F. R. Greten. 2005. NF-κB: linking inflammation and immunity to cancer development and progression. Nat. Rev. Immunol. 5:749-759.
4. Zhang, J., B. Shen, and A. Lin. 2007. Novel strategies for inhibition of the p38 MAPK pathway. Trends Pharmacol. Sci. 28:286-295.
5. Schieven, G. L. 2005. The biology of p38 kinase: a central role in inflammation. Curr. Top. Med. Chem. 5:921-928.
6. Schaeffer, V., J. Cuschieri, I. Garcia, M. Knoll, J. Billgren, S. Jelacic, E. Bulger, and R. Maier. 2007. The priming effect of C5a on monocytes is predominantly mediated by the p38 MAPK pathway. Shock. 27:623-630.
7. Tenhunen, O., J. Rysa, M. Ilves, Y. Soini, H. Ruskoaho, and H. Leskinen. 2006. Identification of cell cycle regulatory and inflammatory genes as predominant targets of p38 mitogen-activated protein kinase in the heart. Circ. Res. 99:485-493.
8. Li, Z., J. Y. Ma, I. Kerr, S. Chakravarty, S. Dugar, G. Schreiner, and A. A. Protter. 2006. Selective inhibition of p38alpha MAPK improves cardiac function and reduces myocardial apoptosis in rat model of myocardial injury. Am. J. Physiol. Heart Circ. Physiol. 291:1972-1977.
9. Liu, Y. H., D. Wang, N. E. Rhaleb, X. P. Yang, J. Xu, S. S. Sankey, A. E. Rudolph, and O. A. Carretero. 2005. Inhibition of p38 mitogen-activated protein kinase protects the heart against cardiac remodeling in mice with heart failure resulting from myocardial infarction. J. Card. Fail. 11:74-81.
10. See, F., W. Thomas, K. Way, A. Tzanidis, A. Kompa, D. Lewis, S. Itescu, and H. Krum. 2004. p38 mitogen-activated protein kinase inhibition improves cardiac function and attenuates left ventricular remodeling following myocardial infarction in the rat. J. Am. Coll. Cardiol. 44:1679-1689.
11. Engel, F. B., P. C. Hsieh, R. T. Lee, and M. T. Keating. 2006. FGF1/p38 MAP kinase inhibitor therapy induces cardiomyocyte mitosis, reduces scarring, and rescues function after myocardial infarction. Proc. Natl. Acad. Sci. U. S. A 103: 15546-15551.
12. Gorog, D. A., M. Tanno, X. Cao, M. Bellahcene, R. Bassi, A. M. Kabir, K. Dighe, R. A. Quinlan, and M. S. Marber. 2004. Inhibition of p38 MAPK activity fails to attenuate contractile dysfunction in a mouse model of low-flow ischemia. Cardiovasc. Res. 61:123-131.
13. Behr, T. M., S. S. Nerurkar, A. H. Nelson, R. W. Coatney, T. N. Woods, A. Sulpizio, S. Chandra, D. P. Brooks, S. Kumar, J. C. Lee, E. H. Ohlstein, C. E. Angermann, J. L. Adams, J. Sisko, J. D. Sackner-Bernstein, and R. N. Willette. 2001. Hypertensive end-organ damage and premature mortality are p38 mitogen-activated protein kinase-dependent in a rat model of cardiac hypertrophy and dysfunction. Circulation. 104:1292-1298.
14. Ma, X. L., S. Kumar, F. Gao, C. S. Louden, B. L. Lopez, T. A. Christopher, C. Wang, J. C Lee., G. Z. Feuerstein, and T. L. Yue. 1999. Inhibition of p38 mitogen-activated protein kinase decreases cardiomyocyte apoptosis and improves cardiac function after myocardial ischemia and reperfusion. Circulation. 99: 1685-1691.
15. Fijen, J. W., J. G. Zijlstra, P. De Boer, R. Spanjersberg, J. W. Tervaert, T. S. Vann Der Werf, J. J. Lighterberg, and J. E. Tulleken. 2001. Suppression of the clinical and cytokine response to endotoxin by RWJ-67657, a p38 mitogen-activated protein-kinase inhibitor, in healthy human volunteers. Clin. Exp. Immunol. 124:16-20.
16. Krum, H. 2001. New and emerging pharmacological strategies in the management of chronic heart failure. Curr. Opin. Pharmacol. 1:126-133.
17. Theiss, A. L., J. G. Simmons, C. Jobin, and P. K. Lund. 2005. Tumor necrosis factor TNFα increases collagen accumulation and proliferation in intestinal myofibroblasts via TNF receptor 2. Biol. Chem. 280:36099-36109.
18. Muchaneta-Kubara, E. C., and A. M. El Nahas. 1997. Myofibroblast phenotypes expression in experimental renal scarring. Nephrol. Dial. Transplant. 12:904-915.
19. Hudon-David, F., F. Bouzeghrane, P. Couture, and G. Thibault. 2007. Thy-1 expression by cardiac fibroblasts: lack of association with myofibroblast contractile markers. J. Mol. Cell Cardiol. 42:991-1000.
20. Deblois, D., B. S. Tea, D. Beaudry, and P. Hamet. 2005. Regulation of therapeutic apoptosis: a potential target in controlling hypertensive organ damage. Can. J. Physiol. Pharmacol. 83:29-41.
21. Heeneman, S., J. P. Cleutjens, B. C. Faber, E. E. Creemers, R. J. van Suylen, E. Lutgens, K. B. Cleutjens, and M. J. Daemen. 2003. The dynamic extracellular matrix: intervention strategies during heart failure and atherosclerosis. J. Pathol. 200:516-525.
22. Kimura, H., K. Shintani-Ishida, M. Nakajima, S. Liu, K. Matsumoto, and K. Yoshida. 2006. Ischemic preconditioning or p38 MAP kinase inhibition attenuates myocardial TNFα production and mitochondria damage in brief myocardial ischemia. Life Sci. 78:1901-1910.