ArticleThe Biochemical journal2002
Up-regulation of c-jun mRNA in cardiac myocytes requires the extracellular signal-regulated kinase cascade, but c-Jun N-terminal kinases are required for efficient up-regulation of c-Jun protein.
Article in The Biochemical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 62 citations in OpenAlex.
- Endothelin-A receptor inhibition after cardiopulmonary bypass: cytokines and receptor activation.The Annals of thoracic surgery · 2008Trial
- Neuroprotective effects of resveratrol on retinal ganglion cells in glaucoma in rodents: A narrative review.Animal models and experimental medicine · 2024Review
- Severe Hyperosmotic Stress Issues an ER Stress-Mediated "Death Sentence" in H9c2 Cells, with p38-MAPK and Autophagy "Coming to the Rescue".Biomedicines · 2022Article
- A bioinformatics approach for identifying potential molecular mechanisms and key genes involved in COVID-19 associated cardiac remodeling.Gene reports · 2021Article
- Endothelin receptor polymorphisms in the cardiovascular system: potential implications for therapy and screening.Heart failure reviews · 2014Article
- Modelling negative feedback networks for activating transcription factor 3 predicts a dominant role for miRNAs in immediate early gene regulation.PLoS computational biology · 2014Article
- Nerve injury-induced c-Jun activation in Schwann cells is JNK independent.BioMed research international · 2014Article
- Regulation of expression of the rat orthologue of mouse double minute 2 (MDM2) by H(2)O(2)-induced oxidative stress in neonatal rat cardiac myocytes.The Journal of biological chemistry · 2009Article
- Regulation of c-Fos and c-Jun gene expression by phospholipase C activity in adult cardiomyocytes.Molecular and cellular biochemistry · 2009Article
- CapZ dynamics are altered by endothelin-1 and phenylephrine via PIP2- and PKC-dependent mechanisms.American journal of physiology. Cell physiology · 2009Article
- Differential roles of MAPKs and MSK1 signalling pathways in the regulation of c-Jun during phenylephrine-induced cardiac myocyte hypertrophy.Molecular and cellular biochemistry · 2009Article
- Endothelin-1 regulates astrocyte proliferation and reactive gliosis via a JNK/c-Jun signaling pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Transient and sustained oxidative stress differentially activate the JNK1/2 pathway and apoptotic phenotype in H9c2 cells.Molecular and cellular biochemistry · 2008Article
- Temporal regulation of expression of immediate early and second phase transcripts by endothelin-1 in cardiomyocytes.Genome biology · 2008Article
- Activin acts with nerve growth factor to regulate calcitonin gene-related peptide mRNA in sensory neurons.Neuroscience · 2007Article
- c-Jun N-terminal kinase is required for vitamin E succinate-induced apoptosis in human gastric cancer cells.World journal of gastroenterology · 2004Article
- Increases in c-Jun N-terminal kinase/stress-activated protein kinase and p38 activity in monocyte-derived macrophages following the uptake of Legionella pneumophila.Infection and immunity · 2004Article
- Chronic mild hypoxia protects heart-derived H9c2 cells against acute hypoxia/reoxygenation by regulating expression of the SUR2A subunit of the ATP-sensitive K+ channel.The Journal of biological chemistry · 2003Article
- Chronic activation of extracellular-signal-regulated protein kinases by phenylephrine is required to elicit a hypertrophic response in cardiac myocytes.The Biochemical journal · 2003Article
- beta-Arrestin-mediated PDE4 cAMP phosphodiesterase recruitment regulates beta-adrenoceptor switching from Gs to Gi.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy, an important adaptational response, is associated with up-regulation of the immediate early gene, c- jun, which encodes the c-Jun transcription factor. c-Jun may feed back to up-regulate its own transcription and, since the c-Jun N-terminal kinase (JNK) family of mitogen-activated protein kinases (MAPKs) phosphorylate c-Jun(Ser-63/73) to increase its transactivating activity, JNKs are thought to be the principal factors involved in c- jun up-regulation. Hypertrophy in primary cultures of cardiac myocytes is induced by endothelin-1, phenylephrine or PMA, probably through activation of one or more of the MAPK family. These three agonists increased c- jun mRNA with the rank order of potency of PMA approximately endothelin-1>phenylephrine. Up-regulation of c- jun mRNA by endothelin-1 was attenuated by inhibitors of protein kinase C (GF109203X) and the extracellular signal-regulated kinase (ERK) cascade (PD98059 or U0126), but not by inhibitors of the JNK (SP600125) or p38-MAPK (SB203580) cascades. Hyperosmotic shock (0.5 M sorbitol) powerfully activates JNKs, but did not increase c- jun mRNA. These data suggest that ERKs, rather than JNKs, are required for c- jun up-regulation. However, endothelin-1 and phenylephrine induced greater up-regulation of c-Jun protein than PMA and phosphorylation of c-Jun(Ser-63/73) correlated with the level of c-Jun protein. Up-regulation of c-Jun protein by endothelin-1 was attenuated by inhibitors of protein kinase C and the ERK cascade, probably correlating with a primary input of ERKs into transcription. In addition, SP600125 inhibited the phosphorylation of c-Jun(Ser-63/73), attenuated the increase in c-Jun protein induced by endothelin-1 and increased the rate of c-Jun degradation. Thus whereas ERKs are the principal MAPKs required for c- jun transcription, JNKs are necessary to stabilize c-Jun for efficient up-regulation of the protein.
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