AJP - Heart Calcium Transients and Cell-Sarcomere
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 280: H1011-H1018, 2001;
0363-6135/01 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (28)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Montgomery, D. E.
Right arrow Articles by Solaro, R. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Montgomery, D. E.
Right arrow Articles by Solaro, R. J.
Vol. 280, Issue 3, H1011-H1018, March 2001

Transgenic incorporation of skeletal TnT into cardiac myofilaments blunts PKC-mediated depression of force

David E. Montgomery1, Murali Chandra1, Qi-Quan Huang2, Jian-Ping Jin2, and R. John Solaro1

1 Program in Cardiovascular Sciences, Department of Physiology and Biophysics, College of Medicine, University of Illinois, Chicago, Illinois 60612; and 2 Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106

Protein kinase C (PKC)-mediated phosphorylation of cardiac troponin I (cTnI) and troponin T (cTnT) has been shown to diminish maximum activation of myofilaments. The functional role of cTnI phosphorylation has been investigated. However, the impact of cTnT phosphorylation on myofilament force is not well studied. We tested the effect of endogenous PKC activation on steady-state tension development and Ca2+ sensitivity in skinned fiber bundles from transgenic (TG) mouse hearts expressing fast skeletal TnT (fsTnT), which naturally lacks the PKC sites present in cTnT. The 12-O-tetradecanoylphorbol 13-acetate (TPA) treatment induced a 29% (46.1 ± 2.5 vs. 33.4 ± 2.6 mN/mm2) reduction in maximum tension in the nontransgenic (NTG) preparations (n = 7) and was inhibited with chelerythrine. However, TPA did not induce a change in the maximum tension in the TG preparations (n = 11). TPA induced a small but significant (P < 0.02) increase in Ca2+ sensitivity (untreated pCa50 = 5.63 ± 0.01 vs. treated pCa50 = 5.72 ± 0.01) only in TG preparations. In TG preparations, 32P incorporation was not evident in TnT and was also significantly diminished in cTnI, compared with NTG. Our data indicate that incorporation of fsTnT into the cardiac myofilament lattice blunts PKC-mediated depression of maximum tension. These data also suggest that cTnT may play an important role in amplifying the myofilament depression induced by PKC-mediated phosphorylation of cTnI.

troponin; phosphorylation sites; myofilament activation; protein kinase C


This article has been cited by other articles:


Home page
 Am. J. Physiol. Cell Physiol.Home page
Q.-Q. Huang, H. Z. Feng, J. Liu, J. Du, L. B. Stull, C. S. Moravec, X. Huang, and J.-P. Jin
Co-expression of skeletal and cardiac troponin T decreases mouse cardiac function
Am J Physiol Cell Physiol, January 1, 2008; 294(1): C213 - C222.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
D. E. Montgomery, V. L. M. Rundell, P. H. Goldspink, D. Urboniene, D. L. Geenen, P. P. de Tombe, and P. M. Buttrick
Protein kinase C{varepsilon} induces systolic cardiac failure marked by exhausted inotropic reserve and intact Frank-Starling mechanism
Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H1881 - H1888.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
M. Chandra, M. L. Tschirgi, and J. C. Tardiff
Increase in tension-dependent ATP consumption induced by cardiac troponin T mutation
Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H2112 - H2119.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
P. H. Goldspink, D. E. Montgomery, L. A. Walker, D. Urboniene, R. D. McKinney, D. L. Geenen, R. J. Solaro, and P. M. Buttrick
Protein Kinase C{epsilon} Overexpression Alters Myofilament Properties and Composition During the Progression of Heart Failure
Circ. Res., August 20, 2004; 95(4): 424 - 432.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
J. M. Metzger and M. V. Westfall
Covalent and Noncovalent Modification of Thin Filament Action: The Essential Role of Troponin in Cardiac Muscle Regulation
Circ. Res., February 6, 2004; 94(2): 146 - 158.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
M. P. Sumandea, W. G. Pyle, T. Kobayashi, P. P. de Tombe, and R. J. Solaro
Identification of a Functionally Critical Protein Kinase C Phosphorylation Residue of Cardiac Troponin T
J. Biol. Chem., September 12, 2003; 278(37): 35135 - 35144.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
W. G. Pyle, M. P. Sumandea, R. J. Solaro, and P. P. De Tombe
Troponin I serines 43/45 and regulation of cardiac myofilament function
Am J Physiol Heart Circ Physiol, September 1, 2002; 283(3): H1215 - H1224.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
D. E. Montgomery, B. M. Wolska, W. G. Pyle, B. B. Roman, J. C. Dowell, P. M. Buttrick, A. P. Koretsky, P. Del Nido, and R. J. Solaro
alpha -Adrenergic response and myofilament activity in mouse hearts lacking PKC phosphorylation sites on cardiac TnI
Am J Physiol Heart Circ Physiol, June 1, 2002; 282(6): H2397 - H2405.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online