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Article

Id2 Represses Aldosterone-Stimulated Cardiac T-Type Calcium Channels Expression

1
Laboratory of Animal Cell Physiology, Graduate School of Bioagricultural Sciences, Nagoya University, Aichi 464-8601, Japan
2
Translational Research Unit, Section for Cellular Therapy, Oslo University Hospital, 0379 Oslo, Norway
3
Department of Experimental Genome Research, Research Institute for Microbial Diseases, Osaka 565-0871, Japan
4
Institute for Scientific and Industrial Researches, Osaka University, Osaka 567-0047, Japan
5
Department of Bioengineering, Nagaoka University of Technology, Nagaoka 940-2188, Japan
*
Author to whom correspondence should be addressed.
Present address: Department of Pharmacology, Faculty of Medicine, Osaka Medical College, Osaka 569-8686, Japan.
Academic Editor: Luigi Petramala
Int. J. Mol. Sci. 2021, 22(7), 3561; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073561
Received: 9 March 2021 / Revised: 22 March 2021 / Accepted: 23 March 2021 / Published: 30 March 2021
(This article belongs to the Special Issue Role of Aldosterone Excess in Determining Cardiovascular Risk)
Aldosterone excess is a cardiovascular risk factor. Aldosterone can directly stimulate an electrical remodeling of cardiomyocytes leading to cardiac arrhythmia and hypertrophy. L-type and T-type voltage-gated calcium (Ca2+) channels expression are increased by aldosterone in cardiomyocytes. To further understand the regulation of these channels expression, we studied the role of a transcriptional repressor, the inhibitor of differentiation/DNA binding protein 2 (Id2). We found that aldosterone inhibited the expression of Id2 in neonatal rat cardiomyocytes and in the heart of adult mice. When Id2 was overexpressed in cardiomyocytes, we observed a reduction in the spontaneous action potentials rate and an arrest in aldosterone-stimulated rate increase. Accordingly, Id2 siRNA knockdown increased this rate. We also observed that CaV1.2 (L-type Ca2+ channel) or CaV3.1, and CaV3.2 (T-type Ca2+ channels) mRNA expression levels and Ca2+ currents were affected by Id2 presence. These observations were further corroborated in a heart specific Id2- transgenic mice. Taken together, our results suggest that Id2 functions as a transcriptional repressor for L- and T-type Ca2+ channels, particularly CaV3.1, in cardiomyocytes and its expression is controlled by aldosterone. We propose that Id2 might contributes to a protective mechanism in cardiomyocytes preventing the presence of channels associated with a pathological state. View Full-Text
Keywords: aldosterone; cardiomyocytes; T-type calcium channels (List three to ten pertinent keywords specific to the article yet reasonably common within the subject discipline.) aldosterone; cardiomyocytes; T-type calcium channels (List three to ten pertinent keywords specific to the article yet reasonably common within the subject discipline.)
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MDPI and ACS Style

Ito, J.; Minemura, T.; Wälchli, S.; Niimi, T.; Fujihara, Y.; Kuroda, S.; Takimoto, K.; Maturana, A.D. Id2 Represses Aldosterone-Stimulated Cardiac T-Type Calcium Channels Expression. Int. J. Mol. Sci. 2021, 22, 3561. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073561

AMA Style

Ito J, Minemura T, Wälchli S, Niimi T, Fujihara Y, Kuroda S, Takimoto K, Maturana AD. Id2 Represses Aldosterone-Stimulated Cardiac T-Type Calcium Channels Expression. International Journal of Molecular Sciences. 2021; 22(7):3561. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073561

Chicago/Turabian Style

Ito, Jumpei, Tomomi Minemura, Sébastien Wälchli, Tomoaki Niimi, Yoshitaka Fujihara, Shun’ichi Kuroda, Koichi Takimoto, and Andrés D. Maturana 2021. "Id2 Represses Aldosterone-Stimulated Cardiac T-Type Calcium Channels Expression" International Journal of Molecular Sciences 22, no. 7: 3561. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073561

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