ArticleJournal of molecular and cellular cardiology2007
Regulation of mTOR and S6K1 activation by the nPKC isoforms, PKCepsilon and PKCdelta, in adult cardiac muscle cells.
Article in Journal of molecular and cellular cardiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 54 citations in OpenAlex.
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- Endothelin-1-induced hypertrophic alterations and heme oxygenase-1 expression in cardiomyoblasts are counteracted by beta estradiol: in vitro and in vivo studies.Naunyn-Schmiedeberg's archives of pharmacology · 2018Article
- Co-ordinated activation of classical and novel PKC isoforms is required for PMA-induced mTORC1 activation.PloS one · 2017Article
- Hydrophobic motif site-phosphorylated protein kinase CβII between mTORC2 and Akt regulates high glucose-induced mesangial cell hypertrophy.American journal of physiology. Cell physiology · 2016Article
- mTOR Complexes Repress Hypertrophic Agonist-Stimulated Expression of Connective Tissue Growth Factor in Adult Cardiac Muscle Cells.Journal of cardiovascular pharmacology · 2016Article
- Insulin Signaling in Bupivacaine-induced Cardiac Toxicity: Sensitization during Recovery and Potentiation by Lipid Emulsion.Anesthesiology · 2016Article
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- DAG/PKCδ and IP3/Ca²⁺/CaMK IIβ Operate in Parallel to Each Other in PLCγ1-Driven Cell Proliferation and Migration of Human Gastric Adenocarcinoma Cells, through Akt/mTOR/S6 Pathway.International journal of molecular sciences · 2015Article
- Estrogen-Related Receptor α (ERRα) is required for adaptive increases in PGC-1 isoform expression during electrically stimulated contraction of adult cardiomyocytes in sustained hypoxic conditions.International journal of cardiology · 2015Article
- Calcium handling proteins: structure, function, and modulation by exercise.Heart failure reviews · 2014Article
- Insulin stimulates mitochondrial fusion and function in cardiomyocytes via the Akt-mTOR-NFκB-Opa-1 signaling pathway.Diabetes · 2014Article
- mTOR complex 2 mediates Akt phosphorylation that requires PKCε in adult cardiac muscle cells.Cellular signalling · 2013Article
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- The role of PKCε-dependent signaling for cardiac differentiation.Histochemistry and cell biology · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Activation of both mTOR and its downstream target, S6K1 (p70 S6 kinase) have been implicated to affect cardiac hypertrophy. Our earlier work, in a feline model of 1-48 h pressure overload, demonstrated that mTOR/S6K1 activation occurred primarily through a PKC/c-Raf pathway. To further delineate the role of specific PKC isoforms on mTOR/S6K1 activation, we utilized primary cultures of adult feline cardiomyocytes in vitro and stimulated with endothelin-1 (ET-1), phenylephrine (PE), TPA, or insulin. All agonist treatments resulted in S2248 phosphorylation of mTOR and T389 and S421/T424 phosphorylation of S6K1, however only ET-1 and TPA-stimulated mTOR/S6K1 activation was abolished with infection of a dominant negative adenoviral c-Raf (DN-Raf) construct. Expression of DN-PKC(epsilon) blocked ET-1-stimulated mTOR S2448 and S6K1 S421/T424 and T389 phosphorylation but had no effect on insulin-stimulated S6K1 phosphorylation. Expression of DN-PKC(delta) or pretreatment of cardiomyocytes with rottlerin, a PKC(delta) specific inhibitor, blocked both ET-1 and insulin stimulated mTOR S2448 and S6K1 T389 phosphorylation. However, treatment with Gö6976, a specific classical PKC (cPKC) inhibitor did not affect mTOR/S6K1 activation. These data indicate that: (i) PKC(epsilon) is required for ET-1-stimulated T421/S424 phosphorylation of S6K1, (ii) both PKC(epsilon) and PKC(delta) are required for ET-1-stimulated mTOR S2448 and S6K1 T389 phosphorylation, (iii) PKC(delta) is also required for insulin-stimulated mTOR S2448 and S6K1 T389 phosphorylation. Together, these data delineate both distinct and combinatorial roles of specific PKC isoforms on mTOR and S6K1 activation in adult cardiac myocytes following hypertrophic stimulation.
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