Membrane Proteins | L-Type Calcium Channels in Health and Disease: The Case of Heart Failure

Katat, Aya Al; Segura, Émilie; Parent, Lucie

doi:10.1016/b978-0-12-819460-7.00077-3

Cited by 1 publication

(3 citation statements)

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“…The present study has revealed that in addition to the acute increase in Ca 2+ influx via activation of the L-type Ca V 1.2 channel after sympathetic discharge [ 10 ], chronic NE treatment of NRVMs translated to a sustained increase in Ca 2+ channel activity. The latter response required β 1 -adrenergic receptor-mediated recruitment of the tyrosine kinase ERK1/2 translating to the increased expression of the Ca V 1.2 auxiliary subunit, Ca V α2δ1.…”

Section: Discussionmentioning

confidence: 99%

“…In ventricular cardiomyocytes, voltage-gated L-type Ca 2+ channels (LTCCs) mediate extracellular Ca 2+ entry initiating Ca 2+ -induced Ca 2+ release and triggering cardiac excitation-contraction coupling [ 1 , 9 , 10 ]. LTCC are oligomeric proteins composed of the pore-forming subunit Ca V α1 bound to the auxiliary subunits Ca V β, calmodulin, and Ca V α2δ [ 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

“…In ventricular cardiomyocytes, the major isoforms are Ca V α1C [ 13 , 14 ], Ca V β2 [ 14 , 15 , 16 ], and Ca V α2δ1 [ 17 , 18 ]. Ca V α1C is the pore-forming subunit responsible for Ca 2+ selectivity, activation and inactivation kinetics [ 10 , 19 ]. Ca V β is a cytoplasmic chaperone protein that supports the trafficking of Ca V 1.2 channels to the plasma membrane [ 20 , 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

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Sympathetic Stimulation Upregulates the Ca2+ Channel Subunit, CaVα2δ1, via the β1 and ERK 1/2 Pathway in Neonatal Ventricular Cardiomyocytes

Katat

Zhao

Calderone

et al. 2022

Cells

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Intracellular Ca2+ overload secondary to chronic hemodynamic stimuli promotes the recruitment of Ca2+-dependent signaling implicated in cardiomyocyte hypertrophy. The present study tested the hypothesis that sympathetic-mediated hypertrophy of neonatal rat ventricular cardiomyocytes (NRVMs) translated to an increase in calcium influx secondary to the upregulation of CaV1.2 channel subunits. Confocal imaging of norepinephrine (NE)-treated NRVMs revealed a hypertrophic response compared to untreated NRVMs. L-type CaV1.2 peak current density was increased 4-fold following a 24-h stimulation with NE. NE-treated NRVMs exhibited a significant upregulation of CaVα2δ1 and CaVβ3 protein levels without significant changes of CaVα1C and CaVβ2 protein levels. Pre-treatment with the β1-blocker metoprolol failed to inhibit hypertrophy or CaVβ3 upregulation whereas CaVα2δ1 protein levels were significantly reduced. NE promoted the phosphorylation of ERK 1/2, and the response was attenuated by the β1-blocker. U0126 pre-treatment suppressed NE-induced ERK1/2 phosphorylation but failed to attenuate hypertrophy. U0126 inhibition of ERK1/2 phosphorylation prevented NE-mediated upregulation of CaVα2δ1, whereas CaVβ3 protein levels remained elevated. Thus, β1-adrenergic receptor-mediated recruitment of the ERK1/2 plays a seminal role in the upregulation of CaVα2δ1 in NRVMs independent of the concomitant hypertrophic response. However, the upregulation of CaVβ3 protein levels may be directly dependent on the hypertrophic response of NRVMs.

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Section: Discussionmentioning

confidence: 99%