ArticleThe Journal of biological chemistry2010
ACTH induces Cav3.2 current and mRNA by cAMP-dependent and cAMP-independent mechanisms.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Role of exchange proteins directly activated by cAMP signaling in vascular remodeling.Pharmacological reviews · 2025Review
- The Ion Channel and GPCR Toolkit of Brain Capillary Pericytes.Frontiers in cellular neuroscience · 2020Review
- Primary aldosteronism associated with a germline variant inBMJ case reports · 2019Article
- Intracellular cAMP Sensor EPAC: Physiology, Pathophysiology, and Therapeutics Development.Physiological reviews · 2018Review
- T-Type Calcium Channel: A Privileged Gate for Calcium Entry and Control of Adrenal Steroidogenesis.Frontiers in endocrinology · 2016Review
- Dual Topology of the Melanocortin-2 Receptor Accessory Protein Is Stable.Frontiers in endocrinology · 2016Article
- Adrenal fasciculata cells express T-type and rapidly and slowly activating L-type Ca2+ channels that regulate cortisol secretion.American journal of physiology. Cell physiology · 2015Article
- Ca2+ and K+ channels of normal human adrenal zona fasciculata cells: properties and modulation by ACTH and AngII.The Journal of general physiology · 2013Article
- AKAP-dependent sensitization of Ca(v) 3.2 channels via the EP(4) receptor/cAMP pathway mediates PGE(2) -induced mechanical hyperalgesia.British journal of pharmacology · 2013Article
- Functional chromaffin cell plasticity in response to stress: focus on nicotinic, gap junction, and voltage-gated Ca2+ channels.Journal of molecular neuroscience : MN · 2012Review
- 8-Phenylthio-adenines stimulate the expression of steroid hydroxylases, Cav3.2 Ca²⁺ channels, and cortisol synthesis by a cAMP-independent mechanism.American journal of physiology. Endocrinology and metabolism · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Bovine adrenal zona fasciculata (AZF) cells express Ca(v)3.2 T-type Ca(2+) channels that function pivotally in adrenocorticotropic hormone (ACTH)-stimulated cortisol secretion. The regulation of Ca(v)3.2 expression in AZF cells by ACTH, cAMP analogs, and their metabolites was studied using Northern blot and patch clamp recording. Exposing AZF cells to ACTH for 3-6 days markedly enhanced the expression of Ca(v)3.2 current. The increase in Ca(v)3.2 current was preceded by an increase in corresponding CACNA1H mRNA. O-Nitrophenyl,sulfenyl-adrenocorticotropin, which produces a minimal increase in cAMP, also enhanced Ca(v)3.2 current. cAMP analogs, including 8-bromoadenosine cAMP (600 mum) and 6-benzoyladenosine cAMP (300 mum) induced CACNA1H mRNA, but not Ca(v)3.2 current. In contrast, 8-(4-chlorophenylthio) (8CPT)-cAMP (10-50 mum) enhanced CACNA1H mRNA and Ca(v)3.2 current, whereas nonhydrolyzable Sp-8CPT-cAMP failed to increase either Ca(v)3.2 current or mRNA. Metabolites of 8CPT-cAMP, including 8CPT-adenosine and 8CPT-adenine, increased Ca(v)3.2 current and mRNA with a potency and effectiveness similar to the parent compound. The Epac activator 8CPT-2'-O-methyl-cAMP and its metabolites 8CPT-2'-OMe-5'-AMP and 8CPT-2'-O-methyl-adenosine increased CACNA1H mRNA and Ca(v)3.2 current; Sp-8CPT-2'-O-methyl-cAMP increased neither Ca(v)3.2 current nor mRNA. These results reveal an interesting dichotomy between ACTH and cAMP with regard to regulation of CACNA1H mRNA and Ca(2+) current. Specifically, ACTH induces expression of CACNA1H mRNA and Ca(v)3.2 current in AZF cells by mechanisms that depend at most only partly on cAMP. In contrast, cAMP enhances expression of CACNA1H mRNA but not the corresponding Ca(2+) current. Surprisingly, chlorophenylthio-cAMP analogs stimulate the expression of Ca(v)3.2 current indirectly through metabolites. ACTH and the metabolites may induce Ca(v)3.2 expression by the same, unidentified mechanism.
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