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Thyroid Hormone Upregulates Cav1.2 Channels in Cardiac Cells via the Downregulation of the Channels' ß4 Subunit.
Carrillo, Elba D; Alvarado, Juan A; Hernández, Ascención; Lezama, Ivonne; García, María C; Sánchez, Jorge A.
Affiliation
  • Carrillo ED; Department of Pharmacology, Center for Research and Advanced Studies of the National Polytechnic Institute, Mexico City 07360, Mexico.
  • Alvarado JA; Department of Pharmacology, Center for Research and Advanced Studies of the National Polytechnic Institute, Mexico City 07360, Mexico.
  • Hernández A; Department of Pharmacology, Center for Research and Advanced Studies of the National Polytechnic Institute, Mexico City 07360, Mexico.
  • Lezama I; Department of Pharmacology, Center for Research and Advanced Studies of the National Polytechnic Institute, Mexico City 07360, Mexico.
  • García MC; Department of Pharmacology, Center for Research and Advanced Studies of the National Polytechnic Institute, Mexico City 07360, Mexico.
  • Sánchez JA; Department of Pharmacology, Center for Research and Advanced Studies of the National Polytechnic Institute, Mexico City 07360, Mexico.
Int J Mol Sci ; 25(19)2024 Oct 08.
Article in En | MEDLINE | ID: mdl-39409130
ABSTRACT
Thyroid hormone binds to specific nuclear receptors, regulating the expression of target genes, with major effects on cardiac function. Triiodothyronine (T3) increases the expression of key proteins related to calcium homeostasis, such as the sarcoplasmic reticulum calcium ATPase pump, but the detailed mechanism of gene regulation by T3 in cardiac voltage-gated calcium (Cav1.2) channels remains incompletely explored. Furthermore, the effects of T3 on Cav1.2 auxiliary subunits have not been investigated. We conducted quantitative reverse transcriptase polymerase chain reaction, Western blot, and immunofluorescence experiments in H9c2 cells derived from rat ventricular tissue, examining the effects of T3 on the expression of α1c, the principal subunit of Cav1.2 channels, and Cavß4, an auxiliary Cav1.2 subunit that regulates gene expression. The translocation of phosphorylated cyclic adenosine monophosphate response element-binding protein (pCREB) by T3 was also examined. We found that T3 has opposite effects on these channel proteins, upregulating α1c and downregulating Cavß4, and that it increases the nuclear translocation of pCREB while decreasing the translocation of Cavß4. Finally, we found that overexpression of Cavß4 represses the mRNA expression of α1c, suggesting that T3 upregulates the expression of the α1c subunit in response to a decrease in Cavß4 subunit expression.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Calcium Channels, L-Type / Myocytes, Cardiac Limits: Animals Language: En Journal: Int J Mol Sci Year: 2024 Document type: Article Affiliation country: Mexico Country of publication: Switzerland

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Calcium Channels, L-Type / Myocytes, Cardiac Limits: Animals Language: En Journal: Int J Mol Sci Year: 2024 Document type: Article Affiliation country: Mexico Country of publication: Switzerland