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Protein kinase C zeta regulation of hypertrophic and apoptotic events occurring during rat neonatal heart development and growth.

International journal of immunopathology and pharmacology

Animals, Animals, Newborn, physiology, Apoptosis, Blotting, Western, Cardiomegaly, enzymology, Heart, growth & development, Image Processing, Computer-Assisted, Immunohistochemistry, Immunoprecipitation, In Situ Nick-End Labeling, Microscopy, Immunoelectron, Myocardium, cytology, Protein Kinase C, Rats, Rats, Wistar, Signal Transduction, Transcription Factors

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      Abstract

      The development and growth of the rat heart implies hyperplasia, which stops at birth, and hypertrophy, allowing cardiac mass to grow in response to programmed genetic events along with to haemodynamic overload. Moreover, hypertrophy is accomplished to apoptosis which controls the final number of myocardial cells, deletes vestigial structures, and takes part in remodelling the organ. Since at the basis of all these processes, which lead to the complete development of the heart, the activation of specific signalling pathways underlies, attention has been addressed to the role played in vivo by Protein Kinase C zeta (PKC zeta) in regulating NF-kB signalling system and intrinsic mitochondrial apoptotic route at days 1, 4, 10 and 22 of rat life. In fact, a role has been assigned to PKC zeta in indirectly phosphorylating IKBa, which peaks between 10 and 22 days, through a IKK determining, in turn, NF-kB activation, concomitantly to cytochrome c/Apaf 1 co-localization in the cytoplasm and caspase-9/caspase-3 activation, which leads to the occurrence of apoptosis. Thus a key role for PKC zeta in regulating the hypertrophic and apoptotic events leading to establishment of complete function in rat neonatal heart is here suggested.

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      15698510

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