ArticleMolecular and cellular biochemistry2009
Regulation of c-Fos and c-Jun gene expression by phospholipase C activity in adult cardiomyocytes.
Article in Molecular and cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Mammalian PI-Phospholipase C Isozymes: Structural and Functional Insights and Roles in Health and Disease.Medicina (Kaunas, Lithuania) · 2025Review
- Role of Vasoactive Hormone-Induced Signal Transduction in Cardiac Hypertrophy and Heart Failure.Cells · 2024Review
- Emerging Roles of Phospholipase C Beta Isozymes as Potential Biomarkers in Cardiac Disorders.International journal of molecular sciences · 2023Review
- Upregulation of Phospholipase C Gene Expression Due to Norepinephrine-Induced Hypertrophic Response.Cells · 2022Review
- Scaffold-Mediated Developmental Effects on Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes Are Preserved After External Support Removal.Frontiers in cell and developmental biology · 2021Article
- CDP-Diacylglycerol Synthases (CDS): Gateway to Phosphatidylinositol and Cardiolipin Synthesis.Frontiers in cell and developmental biology · 2020Review
- Sustained phospholipase C stimulation of H9c2 cardiomyoblasts by vasopressin induces an increase in CDP-diacylglycerol synthase 1 (CDS1) through protein kinase C and cFos.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2019Article
- α₁ adrenoceptor activation by norepinephrine inhibits LPS-induced cardiomyocyte TNF-α production via modulating ERK1/2 and NF-κB pathway.Journal of cellular and molecular medicine · 2014Article
- βIIPKC and εPKC isozymes as potential pharmacological targets in cardiac hypertrophy and heart failure.Journal of molecular and cellular cardiology · 2011Review
- Reciprocal regulation of transcription factors and PLC isozyme gene expression in adult cardiomyocytes.Journal of cellular and molecular medicine · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study was undertaken to determine whether gene expression for transcriptional factors such as c-Fos and c-Jun is regulated by phospholipase C (PLC) activity. Norepinephrine (NE) increased PLC beta(1), beta(3), gamma(1), and delta(1) isozyme gene expression, protein contents and their activities in adult rat cardiomyocytes. Increases in PLC beta(1), beta(3), gamma(1), and delta(1) activities and gene expression in response to NE were prevented by prazosin, an alpha(1)-adrenoceptor (AR) antagonist. Furthermore, mRNA levels for c-Fos and c-Jun, unlike other transcriptional factors, were increased by both NE and phenylephrine, a specific alpha(1)-AR agonist. Increases in c-Fos and c-Jun gene expression due to NE were attenuated by both prazosin and a PLC inhibitor, U73122. Activation of protein kinase C (PKC) with phorbol myristate acetate increased c-Fos and c-Jun mRNA, whereas inhibition of PKC with bisindolylmaleimide as well as inhibition of extracellular signal-regulated kinases (ERK) 1/2 with PD98059 abolished the NE-induced increase in c-Fos and c-Jun gene expression. Reduction of c-Jun phosphorylation by SP600125, an inhibitor of JNK activity, was associated with an attenuation of the NE-induced increases in PLC gene expression. It is suggested that c-Fos and c-Jun gene expression is regulated by PLC in adult cardiomyocytes through a PKC- and ERK1/2-dependent pathway.
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