Differential and conditional activation of PKC-isoforms dictates cardiac adaptation during physiological to pathological hypertrophy.

A cardiac hypertrophy is defined as an increase in heart mass which may either be beneficial (physiological hypertrophy) or detrimental (pathological hypertrophy). This study was undertaken to establish the role of different protein kinase-C (PKC) isoforms in the regulation of cardiac adaptation dur...

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Autores principales:	Shaon Naskar, Kaberi Datta, Arkadeep Mitra, Kanchan Pathak, Ritwik Datta, Trisha Bansal, Sagartirtha Sarkar
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/2f34fd95647441ccba14007b6154f010
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spelling	oai:doaj.org-article:2f34fd95647441ccba14007b6154f0102021-11-25T06:05:05ZDifferential and conditional activation of PKC-isoforms dictates cardiac adaptation during physiological to pathological hypertrophy.1932-620310.1371/journal.pone.0104711https://doaj.org/article/2f34fd95647441ccba14007b6154f0102014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/25116170/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203A cardiac hypertrophy is defined as an increase in heart mass which may either be beneficial (physiological hypertrophy) or detrimental (pathological hypertrophy). This study was undertaken to establish the role of different protein kinase-C (PKC) isoforms in the regulation of cardiac adaptation during two types of cardiac hypertrophy. Phosphorylation of specific PKC-isoforms and expression of their downstream proteins were studied during physiological and pathological hypertrophy in 24 week male Balb/c mice (Mus musculus) models, by reverse transcriptase-PCR, western blot analysis and M-mode echocardiography for cardiac function analysis. PKC-δ was significantly induced during pathological hypertrophy while PKC-α was exclusively activated during physiological hypertrophy in our study. PKC-δ activation during pathological hypertrophy resulted in cardiomyocyte apoptosis leading to compromised cardiac function and on the other hand, activation of PKC-α during physiological hypertrophy promoted cardiomyocyte growth but down regulated cellular apoptotic load resulting in improved cardiac function. Reversal in PKC-isoform with induced activation of PKC-δ and simultaneous inhibition of phospho-PKC-α resulted in an efficient myocardium to deteriorate considerably resulting in compromised cardiac function during physiological hypertrophy via augmentation of apoptotic and fibrotic load. This is the first report where PKC-α and -δ have been shown to play crucial role in cardiac adaptation during physiological and pathological hypertrophy respectively thereby rendering compromised cardiac function to an otherwise efficient heart by conditional reversal of their activation.Shaon NaskarKaberi DattaArkadeep MitraKanchan PathakRitwik DattaTrisha BansalSagartirtha SarkarPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 8, p e104711 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Shaon Naskar Kaberi Datta Arkadeep Mitra Kanchan Pathak Ritwik Datta Trisha Bansal Sagartirtha Sarkar Differential and conditional activation of PKC-isoforms dictates cardiac adaptation during physiological to pathological hypertrophy.
description	A cardiac hypertrophy is defined as an increase in heart mass which may either be beneficial (physiological hypertrophy) or detrimental (pathological hypertrophy). This study was undertaken to establish the role of different protein kinase-C (PKC) isoforms in the regulation of cardiac adaptation during two types of cardiac hypertrophy. Phosphorylation of specific PKC-isoforms and expression of their downstream proteins were studied during physiological and pathological hypertrophy in 24 week male Balb/c mice (Mus musculus) models, by reverse transcriptase-PCR, western blot analysis and M-mode echocardiography for cardiac function analysis. PKC-δ was significantly induced during pathological hypertrophy while PKC-α was exclusively activated during physiological hypertrophy in our study. PKC-δ activation during pathological hypertrophy resulted in cardiomyocyte apoptosis leading to compromised cardiac function and on the other hand, activation of PKC-α during physiological hypertrophy promoted cardiomyocyte growth but down regulated cellular apoptotic load resulting in improved cardiac function. Reversal in PKC-isoform with induced activation of PKC-δ and simultaneous inhibition of phospho-PKC-α resulted in an efficient myocardium to deteriorate considerably resulting in compromised cardiac function during physiological hypertrophy via augmentation of apoptotic and fibrotic load. This is the first report where PKC-α and -δ have been shown to play crucial role in cardiac adaptation during physiological and pathological hypertrophy respectively thereby rendering compromised cardiac function to an otherwise efficient heart by conditional reversal of their activation.
format	article
author	Shaon Naskar Kaberi Datta Arkadeep Mitra Kanchan Pathak Ritwik Datta Trisha Bansal Sagartirtha Sarkar
author_facet	Shaon Naskar Kaberi Datta Arkadeep Mitra Kanchan Pathak Ritwik Datta Trisha Bansal Sagartirtha Sarkar
author_sort	Shaon Naskar
title	Differential and conditional activation of PKC-isoforms dictates cardiac adaptation during physiological to pathological hypertrophy.
title_short	Differential and conditional activation of PKC-isoforms dictates cardiac adaptation during physiological to pathological hypertrophy.
title_full	Differential and conditional activation of PKC-isoforms dictates cardiac adaptation during physiological to pathological hypertrophy.
title_fullStr	Differential and conditional activation of PKC-isoforms dictates cardiac adaptation during physiological to pathological hypertrophy.
title_full_unstemmed	Differential and conditional activation of PKC-isoforms dictates cardiac adaptation during physiological to pathological hypertrophy.
title_sort	differential and conditional activation of pkc-isoforms dictates cardiac adaptation during physiological to pathological hypertrophy.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/2f34fd95647441ccba14007b6154f010
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Differential and conditional activation of PKC-isoforms dictates cardiac adaptation during physiological to pathological hypertrophy.

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