Diabetes and thyroid hormones affect connexin-43 and PKC-ε expression in rat heart atria

Title:

Diabetes and thyroid hormones affect connexin-43 and PKC-ε expression in rat heart atria

Creator:

Mitašíková, M., Lin, H., Tomáš Soukup, Imanaga, I., and Narcisa Tribulová

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:19ce9c94-8a2d-4a03-81e5-db334fc2b302
uuid:19ce9c94-8a2d-4a03-81e5-db334fc2b302

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie, srdeční síně, fibrilace síní, diabetologie, physiology, atria of heart, atrial fibrillation, diabetology, connexin-43, PKC-ε, rat heart atria, triiodothyronine, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print

Description:

We have examined the changes of intercellular electrical coupling protein connexin-43 (Cx43) and of PKC-ε in heart atria of diabetic rats and/or after the treatment with triiodothyronine (T3 ). 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 μg/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-ε , were analyzed by Western blots using mouse monoclonal anti-Cx43 and rabbit polyclonal anti-PKC-ε antibodies. We found that the Cx43 expression was significantly increased after the treatment with T3 and in the acute diabetes. Both in diabetes and after T3 treatment the phosphorylation of Cx43 isoforms was markedly suppressed compared to the non-diabetic and T3-untreated controls. Such a down-regulation was less pronounced in diabetic rats after the T3-treatment. The expression of atrial PKC-ε was increased in diabetic rats. This increase was suppressed after T3 administration and the expression was decreased in T3-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., M. Mitašíková ... [et al.]., and Obsahuje seznam literatury

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2009 Volume:58 | Number:2

Harvested from:

CDK

Metadata only:

false