PKC translocation without changes in Gα(q) and PLC-β protein abundance in cardiac hypertrophy and failure

American Journal of Physiology - Heart and Circulatory Physiology

Volumn 277, Issue 6 46-6, 1999, Pages

  Jalili, Thunder ^a,b   Takeishi, Yasuchika ^a   Song, Guojie ^a   Ball, Nancy A ^a   Howles, Gabriel ^a   Walsh, Richard A ^a,c  

^a CASE WESTERN RESERVE UNIVERSITY   (United States)

^b UNIVERSITY OF UTAH   (United States)

^c CASE WESTERN RESERVE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

G proteins; Heart failure; Protein kinase C; Regulators of G protein signaling

Indexed keywords

GUANINE NUCLEOTIDE BINDING PROTEIN; PHOSPHOLIPASE C; PROTEIN KINASE C;

ADOLESCENT; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONGESTIVE HEART FAILURE; CONTROLLED STUDY; ENZYME ACTIVITY; GUINEA PIG; HEART FAILURE; HEART HYPERTROPHY; IMMUNOBLOTTING; LUNG CONGESTION; MALE; NONHUMAN; PATHOGENESIS; PRIORITY JOURNAL; PROTEIN EXPRESSION; SIGNAL TRANSDUCTION;

EID: 0033393697     PISSN: 03636135     EISSN: None     Source Type: Journal    
DOI: 10.1152/ajpheart.1999.277.6.h2298     Document Type: Article

References (27)

1. Akhter, S. A., L. M. Luttrell, H. A. Rockman, G. Iaccarino, R. J. Lefkowitz, and W. J. Koch. Targeting the receptor-Gq interface to inhibit in vivo pressure overload myocardial hypertrophy. Science 280: 574-577, 1998.
2. Berstein, G., J. L. Blank, D. Y. Jhon, J. H. Exton, S. G. Rhee, and E. M. Ross. Phospholipase C-β 1 is a GTPase-activating protein for Gq/11, its physiologic regulator. Cell 70: 411-418, 1992.
3. 2+ sensitive isoforms in the failing human heart. Circulation 99: 384-391, 1999.
4. Chien, K. R., K. U. Knowlton, H. Zhu, and S. Chien. Regulation of cardiac gene expression during myocardial growth and hypertrophy: molecular studies of an adaptive physiologic response. FASEB J. 5: 3037-3046, 1991.
5. Collins, J. F., C. Pawloski-Dahm, M. G. Davis, N. Ball, G. W. Dorn, and R. A. Walsh. The role of the cytoskeleton in left ventricular pressure overload hypertrophy and failure. J. Mol. Cell. Cardiol. 28: 1435-1443, 1996.
6. D'Angelo, D. D., Y. Sakata, J. N. Lorenz, G. P. Boivin, R. A. Walsh, S. B. Liggett, and G. W. Dorn. Transgenic Gaq overexpression induces cardiac contractile failure in mice. Proc. Natl. Acad. Sci. USA 94: 8121-8126, 1997.
7. Gu, X., and S. P. Bishop. Increased protein kinase C and isozyme redistribution in pressure-overload cardiac hypertrophy in the rat. Circ. Res. 75: 926-931, 1994.
8. Hepler, J. R., D. M. Berman, A. G. Gilman, and T. Kozasa. RGS4 and GAIP are GTPase-activating proteins for Gqα and block activation of phospholipase C β by gamma-thio-GTP-Gqα. Proc. Natl. Acad. Sci. USA 94: 428-432, 1997.
9. Heximer, S. P., N. Watson, M. E. Linder, K. J. Blumer, and J. R. Hepler. RGS2/G0S8 is a selective inhibitor of Gqα function. Proc. Natl. Acad. Sci. USA 94: 14389-14393, 1997.
10. Hunter, T., and M. Karin. The regulation of transcription by phosphorylation. Cell 70: 375-387, 1992.
11. Iwasa, Y., and M. M. Hosey. Phosphorylation of cardiac sarcolemma proteins by the calcium-activated phospholipid-dependent protein kinase. J. Biol. Chem. 259: 534-540, 1984.
12. Ju, H., S. Zhao, P. S. Tappia, V. Panagia, and I. M. Dixon. Expression of Gqα and PLC-β in scar and border tissue in heart failure due to myocardial infarction. Circulation 97: 892-899, 1998.
13. Kariya, K., L. R. Karns, and P. C. Simpson. Expression of a constitutively activated mutant of the beta-isozyme of protein kinase C in cardiac myocytes stimulates the promoter of the β-myosin heavy chain isogene. J. Biol. Chem. 266: 10023-10026, 1991.
14. Karns, L. R., K. Kariya, and P. C. Simpson. M-CAT, CArG, and Sp1 elements are required for α1-adrenergic induction of the skeletal alpha-actin promoter during cardiac myocyte hypertrophy. Transcriptional enhancer factor-1 and protein kinase C as conserved transducers of the fetal program in cardiac growth. J. Biol. Chem. 270: 410-417, 1995.
15. 2+ transport and mechanics in compensated pressure-overload hypertrophy and congestive heart failure. Circ. Res. 77: 759-764, 1995.
16. Paul, K., N. A. Ball, G. W. Dorn, and R. A. Walsh. Left ventricular stretch stimulates angiotensin II-mediated phosphatidylinositol hydrolysis and protein kinase C ε isoform translocation in adult guinea pig hearts. Circ. Res. 81: 643-650, 1997.
17. Ping, P., H. Takano, J. Zhang, X. L. Tang, Y. Qiu, R. C. X. Li, S. Banerjee, B. Dawn, Z. Balafonova, and R. Bolli. Isoform-selective activation of protein kinase C by nitric oxide in the heart of conscious rabbits. A signal mechanism for both nitric oxide-induced and ischemia-induced preconditioning. Circ. Res. 84: 587-604, 1999.
18. Ping, P., J. Zhang, Y. Qui, X. L. Tang, S. Manchikalapudi, X. Cao, and R. Bolli. Ischemic preconditioning induces selective translocation of protein kinase C isoforms ε and η in the heart of conscious rabbits without subcellular redistribution of total protein kinase C activity. Circ. Res. 81: 404-414, 1997.
19. Sato, Y., D. G. Ferguson, H. Sako, G. W. Dorn, V. J. Kadambi, A. Yatani, B. D. Hoit, R. A. Walsh, and E. G. Kranias. Cardiac-specific overexpression of mouse cardiac calsequestrin is associated with depressed cardiovascular function and hypertrophy in transgenic mice. J. Biol. Chem. 273: 28470-28477, 1998.
20. Shubeita, H. E., E. A. Martinson, M. van Bilsen, K. R. Chien, and J. H. Brown. Transcriptional activation of the cardiac myosin light chain 2 and atrial natriuretic factor genes by protein kinase C in neonatal rat ventricular myocytes. Proc. Natl. Acad. Sci. USA 89: 1305-1309, 1992.
21. Sugden, P. H., and M. A. Bogoyevitch. Intracellular signaling through protein kinases in the heart. Cardiovasc. Res. 30: 478-492, 1995.
22. Takeishi, Y., G. Chu, D. M. Kirkpatrick, Z. Li, H. Wakasaki, E. G. Kranias, G. L. King, and R. A. Walsh. In vivo phosphorylation of cardiac troponin I by PKCβ2 decreases cardiomyocyte calcium responsiveness and contractility in transgenic mouse hearts. J. Clin. Invest. 102: 72-78, 1998.
23. Trilivas, I., P. M. McDonough, and J. H. Brown. Dissociation of protein kinase C redistribution from the phosphorylation of its substrates. J. Biol. Chem. 266: 8431-8438, 1991.
24. Wakasaki, H., D. Koya, F. J. Schoen, M. R. Jirousek, D. K. Ways, B. D. Hoit, R. A. Walsh, and G. L. King. Targeted overexpression of protein kinase C β2 isoform in myocardium causes cardiomyopathy. Proc. Natl. Acad. Sci. USA 94: 9320-9325, 1997.
25. Zamponi, G. W., E. Bourinet, D. Nelson, J. Nargeot, and T. P. Snutch. Crosstalk between G proteins and protein kinase C mediated by the calcium channel α1 subunit. Nature 385: 442-446, 1997.
26. Zhang, S., N. Watson, J. Zahner, J. N. Rottman, K. J. Blumer, and A. J. Muslin. RGS3 and RGS4 are GTPase activating proteins in the heart. J. Mol. Cell. Cardiol. 30: 269-276, 1998.
27. Zou, Y., I. Komuro, T. Yamazaki, R. Aikawa, S. Kudoh, I. Shiojima, Y. Hiroi, T. Mizuno, and Y. Yazaki. Protein kinase C, but not tyrosine kinase or Ras, plays a critical role in angiotensin Il-induced activation of Raf-1 kinase and extracellular signal-regulated protein kinases in cardiac myocytes. J. Biol. Chem. 271: 3592-3597, 1996.