NDLI: Interventricular differences in myofilament function in experimental congestive heart failure

Content Provider	Springer Nature Link
Author	Belin, Rashad J. Sumandea, Marius P. Sievert, Gail A. Harvey, Laura A. Geenen, David L. Solaro, R. John Tombe, Pieter P.
Copyright Year	2011
Abstract	This study was conducted to identify molecular mechanisms which explain interventricular differences in myofilament function in experimental congestive heart failure (CHF). CHF was induced in rats by chronic aortic banding or myocardial infarction for 32–36 weeks. Right and left ventricular (RV, LV) myocytes were mechanically isolated, triton-skinned, and attached to a force transducer and motor arm. Myofilament force–[Ca2+] relations assessed maximal Ca2+-saturated force (F max) and the [Ca2+] at 50% of F max (EC50). Myofilament protein phosphorylation was determined via ProQ diamond phospho-staining. Protein kinase C (PKC)-α expression/activation and site-specific phosphorylation of cardiac troponin I (cTnI) and cardiac troponin T (cTnT) were measured via immunoblotting. Relative to controls, failing RV myocytes displayed a ~45% decrease in F max with no change in EC50, whereas failing LV myocytes displayed a ~45% decrease in F max and ~50% increase in EC50. Failing LV myofilaments were less Ca2+-sensitive (37% increase in EC50) than failing RV myofilaments. Expression and activation of PKC-α was increased twofold in failing RV myocardium and relative to the RV, PKC-α was twofold higher in the failing LV, while PKC-β expression was unchanged by CHF. PKC-α-dependent phosphorylation and PP1-mediated dephosphorylation of failing RV myofilaments increased EC50 and increased F max, respectively. Phosphorylation of cTnI and cTnT was greater in failing LV myofilaments than in failing RV myofilaments. RV myofilament function is depressed in experimental CHF in association with increased PKC-α signaling and myofilament protein phosphorylation. Furthermore, myofilament dysfunction is greater in the LV compared to the RV due in part to increased PKC-α activation and phosphorylation of cTnI and cTnT.
Starting Page	795
Ending Page	809
Page Count	15
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	462
Issue Number	6
e-ISSN	14322013
Language	English
Publisher	Springer-Verlag
Publisher Date	2011-09-17
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Heart Muscle mechanics Force–pCa relation Myofilaments Protein kinase C Hypertrophy Human Physiology
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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Interventricular differences in myofilament function in experimental congestive heart failure

Augmented protein kinase C-alpha-induced myofilament protein phosphorylation contributes to myofilament dysfunction in experimental congestive heart failure.

Protein phosphorylation contributes to myofilament dysfunction in experimental congestive heart failure (2007).

Diastolic myofilament dysfunction in the failing human heart

Protein kinase C α and ε phosphorylation of troponin and myosin binding protein C reduce Ca2+ sensitivity in human myocardium

Diastolic myofilament dysfunction in the failing human heart

Heart failure-specific changes in protein kinase signalling

Myofilament dysfunction in cardiac disease from mice to men

Protein kinase C in heart failure: a therapeutic target?

Interventricular differences in myofilament function in experimental congestive heart failure

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Interventricular differences in myofilament function in experimental congestive heart failure

Augmented protein kinase C-alpha-induced myofilament protein phosphorylation contributes to myofilament dysfunction in experimental congestive heart failure.

Protein phosphorylation contributes to myofilament dysfunction in experimental congestive heart failure (2007).

Diastolic myofilament dysfunction in the failing human heart

Protein kinase C α and ε phosphorylation of troponin and myosin binding protein C reduce Ca2+ sensitivity in human myocardium

Diastolic myofilament dysfunction in the failing human heart

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Interventricular differences in myofilament function in experimental congestive heart failure