Molecular basis for the modulation  of native T-type Ca2+ channels in vivo by Ca2+/calmodulin-dependent protein kinase II

Yao, Jian

doi:10.1172/jci27918

Cited by 43 publications

(44 citation statements)

References 56 publications

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“…In ZG cells, both extracellular K + and Ang II increased oscillation frequency. We postulate that K + -induced depolarization moves the baseline Vm of the ZG cell into a voltage range of enhanced Cav3.2 steady-state window current and that Ang II, by its known actions to induce a hyperpolarizing shift in the voltage dependence of Cav3.2 channels (45)(46)(47)(48), expands the voltage region of steady-state window current expression.…”

Section: Discussionmentioning

confidence: 93%

Zona glomerulosa cells of the mouse adrenal cortex are intrinsic electrical oscillators

Hu¹,

Rusin²,

Tan³

et al. 2012

J. Clin. Invest.

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Aldosterone, which plays a central role in the regulation of blood pressure, is produced by zona glomerulosa (ZG) cells of the adrenal gland. When dysregulated, aldosterone is pathogenic and contributes to the development and progression of cardiovascular and renal disease. Although sustained production of aldosterone requires persistent Ca 2+ entry through low-voltage activated Ca 2+ channels, isolated ZG cells are considered nonexcitable, with recorded membrane voltages that are too hyperpolarized to permit Ca 2+ entry. Here, we show that mouse ZG cells within adrenal slices spontaneously generate membrane potential oscillations of low periodicity. This innate electrical excitability of ZG cells provides a platform for the production of a recurrent Ca 2+ signal that can be controlled by Ang II and extracellular potassium, the 2 major regulators of aldosterone production. We conclude that native ZG cells are electrical oscillators, and that this behavior provides what we believe to be a new molecular explanation for the control of Ca 2+ entry in these steroidogenic cells.

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Section: Discussionmentioning

confidence: 93%

Zona glomerulosa cells of the mouse adrenal cortex are intrinsic electrical oscillators

Hu¹,

Rusin²,

Tan³

et al. 2012

J. Clin. Invest.

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“…T-type Ca 2+ channels are highly expressed in many developing tissues and are implicated in regulating cellular events leading to cell proliferation and differentiation (50). Calcium influx through T-type Ca 2+ channels activates several cellular pathways, including calcineurin/NFAT (29,39), extracellular signal-regulated kinase (31,(51)(52)(53), nitric oxide synthase 3 (54), and Ca 2+ /calmodulindependent protein kinase II (55). However, the detailed mechanisms linking these T-type Ca 2+ channel-activated signaling pathways to cell proliferation and differentiation are not completely clear.…”

Section: Discussionmentioning

confidence: 99%

Ca _v 3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage

Lin

Tzeng

Lee

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Significance The tracheal cartilage rings are important for protecting and maintaining the airway. However, the chondrogenesis of tracheal cartilage is not completely understood. We demonstrate that the Ca v 3.2 T-type calcium channel is required for normal tracheal cartilage ring formation. Calcium influx via Ca v 3.2 induces chondrogenesis and up-regulates a chondrogenic master gene, sex determination region of Y chromosome (SRY)-related high-mobility group-Box gene 9 (Sox9), via a calcium and calcineurin-dependent pathway. Ca v 3.2-dependent regulation of Sox9 is mediated by a newly identified nuclear factor of activated T-cell binding site on the Sox9 promoter. Our study provides novel insight into the roles of Ca v 3.2 T-type calcium channels in tracheal development. Moreover, CACNA1H , the human homolog of the mouse Ca v 3.2-encoding gene, may be a potential candidate gene involved in congenital tracheal stenosis in humans.

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“…Several putative PKC consensus motifs localize to the II-III linker in Ca V 3 channels (Monteil et al, 2000), which could be involved in their regulation by this enzyme . It is noteworthy that the II-III connecting loop is also a critical determinant in the protein kinase A-, calcium/calmodulin-dependent kinase II-, and Rho-associated kinase-mediated modulation of Ca V 3 channels (Kim et al, 2006;Yao et al, 2006;Iftinca et al, 2007). The observed inhibition of Ca V 3.2 channels by NKA is probably not related to a change in the number of channels in the membrane, because the relatively rapid onset and reversal of the NKA modulation (Fig.…”

Section: Nk1 Receptor Modulates Ca V 32 207mentioning

confidence: 92%

Protein Kinase C-Mediated Inhibition of Recombinant T-Type Ca_V3.2 Channels by Neurokinin 1 Receptors

Rangel¹,

Sánchez‐Armass²,

Meza³

2009

Mol Pharmacol

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The voltage-activated T-type calcium channel (Ca V 3.2) and the G protein-coupled neurokinin 1 (NK1) receptor are expressed in peripheral tissues and in central neurons, in which they participate in diverse physiological processes, including neurogenic inflammation and nociception. In the present report, we demonstrate that recombinant Ca V 3.2 channels are reversibly inhibited by NK1 receptors when both proteins are transiently coexpressed in human embryonic kidney 293 cells. We found that the voltage-dependent macroscopic properties of Ca V 3.2 currents were unaffected during NK1 receptor-mediated inhibition. However, inhibition was attenuated in cells coexpressing either the dominant-negative G␣ q Q209L/D277N or the regulator of G protein signaling (RGS) proteins 2 (RGS2) and 3T (RGS3T), which are effective antagonists of G␣ q/11 . By contrast, inhibition was unaffected in cells coexpressing human rod transducin (G␣ t ), which buffers G␤␥. Channel inhibition was blocked by 1-[6-[[17␤-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione (U73122) and bisindolylmaleimide I, selective inhibitors of phospholipase C␤ and protein kinase C (PKC), respectively. Inhibition was occluded by application of the PKC activator phorbol-12-myristate-13-acetate. Altogether, these data indicate that NK1 receptors inhibit Ca V 3.2 channels through a voltage-independent signaling pathway that involves G␣ q/11 , phospholipase C␤, and PKC. Our results provide novel evidence regarding the mechanisms underlying T-type calcium channel modulation by G protein-coupled receptors. Functional coupling between Ca V 3.2 channels and NK1 receptors may be relevant in neurogenic inflammation, neuronal rhythmogenesis, nociception, and other physiological processes.

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Molecular basis for the modulation of native T-type Ca2+ channels in vivo by Ca2+/calmodulin-dependent protein kinase II

Cited by 43 publications

References 56 publications

Zona glomerulosa cells of the mouse adrenal cortex are intrinsic electrical oscillators

Zona glomerulosa cells of the mouse adrenal cortex are intrinsic electrical oscillators

Ca _v 3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage

Protein Kinase C-Mediated Inhibition of Recombinant T-Type Ca_V3.2 Channels by Neurokinin 1 Receptors

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Molecular basis for the modulation of native T-type Ca2+ channels in vivo by Ca2+/calmodulin-dependent protein kinase II

Cited by 43 publications

References 56 publications

Zona glomerulosa cells of the mouse adrenal cortex are intrinsic electrical oscillators

Zona glomerulosa cells of the mouse adrenal cortex are intrinsic electrical oscillators

Ca v 3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage

Protein Kinase C-Mediated Inhibition of Recombinant T-Type CaV3.2 Channels by Neurokinin 1 Receptors

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Product

Resources

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Ca _v 3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage

Protein Kinase C-Mediated Inhibition of Recombinant T-Type Ca_V3.2 Channels by Neurokinin 1 Receptors