RGD Reference Report - Proliferation of neonatal cardiomyocytes by connexin43 knockdown via synergistic inactivation of p38 MAPK and increased expression of FGF1. - Rat Genome Database

Send us a Message
Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   
Search RGD Grant Resources Citing RGD About Us Contact Us
Genes Variants Community Projects QTLs Strains Markers Genome Information Ontologies Cell Lines References Download Submit Data
OntoMate (Literature Search) JBrowse (Genome Browser) Synteny Browser (VCMap) Variant Visualizer Multi-Ontology Enrichment (MOET) Gene-Ortholog Location Finder (GOLF) InterViewer (Protein-Protein Interactions) PhenoMiner (Quatitative Phenotypes) Gene Annotator OLGA (Gene List Generator) AllianceMine GViewer (Genome Viewer)
Aging & Age-Related Disease Cancer & Neoplastic Disease Cardiovascular Disease Coronavirus Disease Developmental Disease Diabetes Hematologic Disease Immune & Inflammatory Disease Infectious Disease Liver Disease Neurological Disease Obesity & Metabolic Syndrome Renal Disease Respiratory Disease Sensory Organ Disease
Find Models   new Genetic Models Autism Models Rat PhenoMiner (Quantitative Phenotypes) Chinchilla PhenoMiner Expected Ranges (Quantitative Phenotype) PhenoMiner Term Comparison Hybrid Rat Diversity Panel Phenotypes Phenotypes in Other Animal Models Animal Husbandry Strain Medical Records Phylogenetics Strain Availability Calendar Rats 101 Submissions Photo Archive
Pathways
Rat Community Forum Directory of Rat Laboratories Video Tutorials News RGD Publications RGD Presentations Archive Nomenclature Guidelines Resource Links Laboratory Resources Employment Resources

Proliferation of neonatal cardiomyocytes by connexin43 knockdown via synergistic inactivation of p38 MAPK and increased expression of FGF1.

Authors: Matsuyama, D  Kawahara, K 
Citation: Matsuyama D and Kawahara K, Basic Res Cardiol. 2009 Nov;104(6):631-42. doi: 10.1007/s00395-009-0029-z. Epub 2009 Apr 18.
RGD ID: 7207421
Pubmed: PMID:19377854   (View Abstract at PubMed)
DOI: DOI:10.1007/s00395-009-0029-z   (Journal Full-text)

Gap junctions are intercellular channels that connect the cytoplasm of adjacent cell. Gap junctional intercellular communication has long been postulated to contribute to the maintenance of tissue homeostasis. Recent studies, however, have demonstrated that connexins, gap junction proteins, are involved in the regulation of a variety of cellular functions other than intercellular communication. Although, in neonatal rat ventricular myocytes, connexin-40, -43, and -45 are all expressed, connexin43 (Cx43) is the primary subtype. In this study, we examined whether and if so how the knockdown of a gap junction protein Cx43 with siRNA produced changes in the proliferative activity of neonatal cardiomyocytes. Cx43-knockdown resulted in a significant increase in the proliferation of cardiomyocytes. To clarify the mechanisms behind this increase, we investigated whether the activity of mitogen-activated protein kinases (MAPKs) changed on knockdown of Cx43. The knockdown decreased the expression of phosphorylated p38 (p-p38) MAPK. In addition, treatment of cardiomyocytes with a p38 MAPK inhibitor significantly increased the proliferative activity. Cultures were then co-treated with an inhibitor of p38 MAPK and fibroblast growth factor-1 (FGF1), since Cx43-knockdown significantly increased cytosolic FGF1 expression as well. The co-treatment enhanced the proliferation of cardiomyocytes compared with the treatment with the p38 MAPK inhibitor alone. Taken together, the present study demonstrated that Cx43-knockdown produced a significant increase in the proliferation of neonatal cardiomyocytes.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
negative regulation of cardiac muscle cell proliferation  IMP 7207421 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Gja1  (gap junction protein, alpha 1)


Additional Information