Enhanced BDNF Actions Following Acute Hypoxia Facilitate HIF-1α-Dependent Upregulation of Cav3-T-Type Ca2+ Channels in Rat Cardiomyocytes

Brain-derived neurotrophic factor (BDNF) has recently been recognized as a cardiovascular regulator particularly in the diseased condition, including coronary artery disease, heart failure, cardiomyopathy, and hypertension. Here, we investigate the role of BDNF on the T-type Ca2+ channel, Cav3.1 and...

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Published in:Membranes (Basel) 2021-06, Vol.11 (7), p.470
Main Authors: Morishima, Masaki, Fujita, Takafumi, Osagawa, Satoshi, Kubota, Hiroshi, Ono, Katsushige
Format: Article
Language:English
Subjects:
BDNF
Brain-derived neurotrophic factor
Calcium channels
Calcium channels (T-type)
Calcium channels (voltage-gated)
Calcium ions
Cardiomyocytes
Cardiomyopathy
Cav3.1
Cav3.2
Channels
Congestive heart failure
Coronary artery
Coronary artery disease
Gene expression
Heart attacks
HIF-1α
Hypertension
Hypoxia
Hypoxia-inducible factor 1a
Investigations
Ischemia
Kinases
Neonates
Proteins
siRNA
T-type Ca2+ channel
TrkB
TrkB receptors
Tropomyosin
Up-regulation
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description Brain-derived neurotrophic factor (BDNF) has recently been recognized as a cardiovascular regulator particularly in the diseased condition, including coronary artery disease, heart failure, cardiomyopathy, and hypertension. Here, we investigate the role of BDNF on the T-type Ca2+ channel, Cav3.1 and Cav3.2, in rat neonatal cardiomyocytes exposed to normoxia (21% O2) and acute hypoxia (1% O2) in vitro for up to 3 h. The exposure of cardiomyocytes to hypoxia (1 h, 3 h) caused a significant upregulation of the mRNAs for hypoxia-inducible factor 1α (Hif1α), Cav3.1, Cav3.2 and Bdnf, but not tropomyosin-related kinase receptor B (TrkB). The upregulation of Cav3.1 and Cav3.2 caused by hypoxia was completely halted by small interfering RNA (siRNA) targeting Hif1a (Hif1a-siRNA) or Bdnf (Bdnf-siRNA). Immunocytochemical staining data revealed a distinct upregulation of Cav3.1- and Cav3.2-proteins caused by hypoxia in cardiomyocytes, which was markedly suppressed by Bdnf-siRNA. These results unveiled a novel regulatory action of BDNF on the T-type Ca2+ channels expression through the HIF-1α-dependent pathway in cardiomyocytes.
doi_str_mv 10.3390/membranes11070470
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subjects BDNF
Brain-derived neurotrophic factor
Calcium channels
Calcium channels (T-type)
Calcium channels (voltage-gated)
Calcium ions
Cardiomyocytes
Cardiomyopathy
Cav3.1
Cav3.2
Channels
Congestive heart failure
Coronary artery
Coronary artery disease
Gene expression
Heart attacks
HIF-1α
Hypertension
Hypoxia
Hypoxia-inducible factor 1a
Investigations
Ischemia
Kinases
Neonates
Proteins
siRNA
T-type Ca2+ channel
TrkB
TrkB receptors
Tropomyosin
Up-regulation
title Enhanced BDNF Actions Following Acute Hypoxia Facilitate HIF-1α-Dependent Upregulation of Cav3-T-Type Ca2+ Channels in Rat Cardiomyocytes
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