ANG II and cardiac myocyte contractility: p38 is not stressed out!

American Journal of Physiology - Heart and Circulatory Physiology

Volumn 290, Issue 1, 2006, Pages

  Sabri, Abdelkarim ^a   Lucchesi, Pamela A ^b  

^a TEMPLE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b LOUISIANA STATE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANGIOTENSIN 2 RECEPTOR; ANGIOTENSIN II; MITOGEN ACTIVATED PROTEIN KINASE 1; MITOGEN ACTIVATED PROTEIN KINASE 3; MITOGEN ACTIVATED PROTEIN KINASE 7; MITOGEN ACTIVATED PROTEIN KINASE KINASE 3; MITOGEN ACTIVATED PROTEIN KINASE P38; PROTEIN KINASE C; PROTEIN TYROSINE KINASE; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE OXIDASE; STRESS ACTIVATED PROTEIN KINASE;

APOPTOSIS; EDITORIAL; ENZYME ACTIVATION; ENZYME PHOSPHORYLATION; EXCITATION CONTRACTION COUPLING; HEART CONTRACTION; HEART FAILURE; HEART MUSCLE CONTRACTILITY; HEART VENTRICLE HYPERTROPHY; HUMAN; IN VIVO STUDY; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; DRUG EFFECT; HEART MUSCLE CELL; NOTE; PHYSIOLOGY;

ANGIOTENSIN II; ENZYME ACTIVATION; MYOCARDIAL CONTRACTION; MYOCYTES, CARDIAC; P38 MITOGEN-ACTIVATED PROTEIN KINASES;

EID: 33644796961     PISSN: 03636135     EISSN: 15221539     Source Type: Journal    
DOI: 10.1152/ajpheart.00873.2005     Document Type: Editorial

References (19)

1. Armstrong SC, Delacey M, and Ganote CE. Phosphorylation state of HSP27 and p38 MAPK during preconditioning and protein phosphatase inhibitor protection of rabbit cardiomyocytes. J Mol Cell Cardiol 31: 555-567, 1999.
2. phox-containing NADPH oxidase in angiotensin II-induced cardiac hypertrophy in mice. Circulation 105: 293-296, 2002.
3. Chen Y, Rajashree R, Liu Q, and Hofmann P. Acute p38 MAPK activation decreases force development in ventricular myocytes. Am J Physiol Heart Circ Physiol 285: H2578-H2586, 2003.
4. Cook SA, Sugden PH, and Clerk A. Activation of c-Jun N-terminal kinases and p38-mitogen-activated protein kinases in human heart failure secondary to ischaemic heart disease. J Mol Cell Cardiol 31: 1429-1434, 1999.
5. 1 receptor induced delayed preconditioning in rabbits: induction of p38 mitogen-activated protein kinase activation and HSP27 phosphorylation via a tyrosine kinase- and protein kinase C-dependent mechanism. Circ Res 86: 989-997, 2000.
6. Hoover HE, Thuerauf DJ, Martindale JJ, and Glembotski CC. αB-crystallin gene induction and phosphorylation by MKK6-activated p38. A potential role for αB-crystallin as a target of the p38 branch of the cardiac stress response. J Biol Chem 275: 23825-23833, 2000.
7. Hu CM, Chen YH, Chiang MT, and Chau LY. Heme oxygenase-1 inhibits angiotensin II-induced cardiac hypertrophy in vitro and in vivo. Circulation 110: 309-316, 2004.
8. Izumiya Y, Kim S, Izumi Y, Yoshida K, Yoshiyama M, Matsuzawa A, Ichijo H, and Iwao H. Apoptosis signal-regulating kinase 1 plays a pivotal role in angiotensin II-induced cardiac hypertrophy and remodeling. Circ Res 93: 874-883, 2003.
9. Kan H, Xie Z, and Finkel MS. p38 MAP kinase-mediated negative inotropic effect of HIV gp120 on cardiac myocytes. Am J Physiol Cell Physiol 286: C1-C7, 2004.
10. Kimura S, Zhang GX, Nishiyama A, Shokoji T, Yao L, Fan YY, Rahman M, Suzuki T, Maeta H, and Abe Y. Role of NAD(P)H oxidase- and mitochondria-derived reactive oxygen species in cardioprotection of ischemic reperfusion injury by angiotensin II. Hypertension 45: 860-866, 2005.
11. Liang Q and Molkentin JD. Redefining the roles of p38 and JNK signaling in cardiac hypertrophy: dichotomy between cultured myocytes and animal models. J Mol Cell Cardiol 35: 1385-1394, 2003.
12. Liao P, Georgakopoulos D, Kovacs A, Zheng M, Lerner D, Pu H, Saffitz J, Chien K, Xiao RP, Kass DA, and Wang Y. The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathy. Proc Natl Acad Sci USA 98: 12283-12288, 2001.
13. Liao P, Wang SQ, Wang GS, Zheng M, Zheng M, Zhang SJ, Cheng H, Wang Y, and Xiao RP. p38 mitogen-activated protein kinase mediates a negative inotropic effect in cardiac myocytes. Circ Res 90: 190-196, 2002.
14. Palomeque J, Sapia L, Hajjar RJ, Mattiazzi A, and Vila Petroff M. Angiotensin II-induced negative inotropy in rat ventricular myocytes: role of reactive oxygen species and p38 MAPK. Am J Physiol Heart Circ Physiol 290: H96-H106, 2006.
15. Petrich BG and Wang Y. Stress-activated MAP kinases in cardiac remodeling and heart failure: new insights from transgenic studies. Trends Cardiovasc Med 14: 50-55, 2004.
16. Sano M, Fukuda K, Sato T, Kawaguchi H, Suematsu M, Matsuda S, Koyasu S, Matsui H, Yamauchi-Takihara K, Harada M, Saito Y, and Ogawa S. ERK and p38 MAPK, but not NF-κB, are critically involved in reactive oxygen species-mediated induction of IL-6 by angiotensin II in cardiac fibroblasts. Circ Res 89: 661-669, 2001.
17. Takeishi Y, HuANGQ, Abe J, Glassman M, Che W, Lee JD, Kawakatsu H, Lawrence EG, Hoit BD, Berk BC, and Walsh RA. Src and multiple MAP kinase activation in cardiac hypertrophy and congestive heart failure under chronic pressure-overload: comparison with acute mechanical stretch. J Mol Cell Cardiol 33: 1637-1648, 2001.
18. 2-terminal kinase in ventricular muscle cells. J Biol Chem 273: 5423-5426, 1998.
19. Wenzel S, Taimor G, Piper HM, and Schluter KD. Redox-sensitive intermediates mediate angiotensin II-induced p38 MAP kinase activation, AP-1 binding activity, and TGF-β expression in adult ventricular cardiomyocytes. FASEB J 15: 2291-2293, 2001.