Diabetes and thyroid hormones affect connexin-43 and PKC-epsilon expression in rat heart atria
Language English Country Czech Republic Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
18380541
DOI
10.33549/physiolres.931425
PII: 1425
Knihovny.cz E-resources
- MeSH
- Diabetes Mellitus, Experimental complications metabolism MeSH
- Atrial Fibrillation complications metabolism MeSH
- Phosphorylation MeSH
- Hyperthyroidism chemically induced complications metabolism MeSH
- Connexin 43 metabolism MeSH
- Blood Glucose metabolism MeSH
- Rats MeSH
- Myocardium metabolism MeSH
- Rats, Inbred WKY MeSH
- Protein Kinase C-epsilon metabolism MeSH
- Heart Atria metabolism MeSH
- Tachycardia, Supraventricular complications metabolism MeSH
- Triiodothyronine pharmacology MeSH
- Up-Regulation physiology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Connexin 43 MeSH
- Blood Glucose MeSH
- Protein Kinase C-epsilon MeSH
- Triiodothyronine MeSH
We have examined the changes of intercellular electrical coupling protein connexin-43 (Cx43) and of PKC-epsilon in heart atria of diabetic rats and/or after the treatment with triiodothyronine (T(3)). Diabetes was induced in Wistar-Kyoto rats by streptozotocin (50 mg/kg, i.v.) and atria were examined after 5 (acute stage) and 10 (chronic stage) weeks. T(3) (10 microg/100 g/day) was applied via a gastric tube for the last 10 days prior to the end of the experiments to non-diabetic and to the half of diabetic rats. Expression and phosphorylated status of Cx43, as well as expression of PKC-epsilon, were analyzed by Western blots using mouse monoclonal anti-Cx43 and rabbit polyclonal anti-PKC-epsilon antibodies. We found that the Cx43 expression was significantly increased after the treatment with T(3) and in the acute diabetes. Both in diabetes and after T(3) treatment the phosphorylation of Cx43 isoforms was markedly suppressed compared to the non-diabetic and T(3)-untreated controls. Such a down-regulation was less pronounced in diabetic rats after the T(3)-treatment. The expression of atrial PKC-epsilon was increased in diabetic rats. This increase was suppressed after T(3) administration and the expression was decreased in T(3)-treated non-diabetic rats. We suggest that the reduced Cx43 phosphorylation in diabetic and hyperthyroid rats can deteriorate a cell-to-cell coupling and consequently facilitate a development of atrial tachyarrhythmia in diabetic or hyperthyroid animals.
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