Abstract：
BACKGROUND:Previous studies suggest that CaMKII activity is required for frequency-dependent acceleration of relaxation (FDAR) in ventricular myocytes. We propose that the underlying mechanism involves CaMKII-dependent regulation of myofilament Ca(2+) sensitivity. METHODS AND RESULTS:Cardiac function was measured in mice using murine echo machine. [Ca(2+)]i and sarcomere length were measured by IonOptix Ca(2+) image system. Increasing pacing rate from 0.5 to 4 Hz in left ventricular myocytes induced frequency-dependent myofilament Ca(2+) desensitization (FDMCD) and FDAR. Acute inhibition of PKA or PKC had no effect, whereas CaMKII inhibition abolished both FDMCD and FDAR. Co-immunoprecipitation of CaMKII and troponin I (TnI) has been detected and CaMKII inhibition significantly reduced serine residue phosphorylation of TnI. Finally, chronic inhibition of CaMKII in vivo reduced TnI phosphorylation and abolished both FDAR and FDMCD, leading to impaired diastolic function. CONCLUSIONS:Our results suggest that CaMKII-dependent TnI phosphorylation is involved in FDMCD and the consequent FDAR and that CaMKII inhibition removes this mechanism and thus induces diastolic dysfunction.
journal_name
Cell Calciumjournal_title
Cell calciumauthors
Guilbert A,Lim HJ,Cheng J,Wang Ydoi
10.1016/j.ceca.2015.08.001subject
Has Abstractpub_date
2015-11-01 00:00:00pages
489-99issue
5eissn
0143-4160issn
1532-1991pii
S0143-4160(15)00127-Xjournal_volume
58pub_type
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