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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 Ca 2+ channel, Cav3.1 and Cav3.2, in rat neonatal cardiomyocytes exposed to normoxia (21% O 2 ) and acute hypoxia (1% O 2 ) 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 ( H  if1  α ), Cav3.1 , Cav3.2 and B  dnf , 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 H  if1  a ( H  if1  a -siRNA) or B  dnf ( B  dnf -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 B  dnf -siRNA. These results unveiled a novel regulatory action of BDNF on the T-type Ca 2+ channels expression through the HIF-1α-dependent pathway in cardiomyocytes.

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