Differential expression by nerve growth factor of two types of Ca2+ channels in rat phaeochromocytoma cell lines.

Usowicz, Maria M.; Porzig, H.; Becker, Charlotte; Réuter, H.

doi:10.1113/jphysiol.1990.sp018128

Cited by 149 publications

(140 citation statements)

References 36 publications

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“…1C shows a representative example of Ca 2ϩ current recorded in a PC12 cell during a depolarizing pulse to ϩ20 mV followed by repolarization to Ϫ70 mV. Consistent with other analyses on Ca 2ϩ currents in PC12 cells (28,29), the recorded current appeared to result predominantly from the expression of HVA and fast deactivating channels, as evidenced by the fast tail current generated when the membrane was repolarized to Ϫ70 mV. The apparent activation threshold of the whole cell Ca 2ϩ current in PC12 cells was observed at about Ϫ50 mV, and maximal current amplitude was observed at ϩ20 mV (see below).…”

Section: Identification Of T-type Ca 2ϩ Channels In Pc12 Cells-pc12supporting

confidence: 65%

“…are chromaffin-like cells that express HVA Ca 2ϩ channels, which have been identified by biophysical and molecular approaches as L-, N-, and P/Q-subtypes (28,29). To our knowledge, T-type Ca 2ϩ channels have not previously been reported in quiescent PC12 cells.…”

Section: Identification Of T-type Ca 2ϩ Channels In Pc12 Cells-pc12mentioning

confidence: 98%

“…Fig. 3 shows real time PCR quantification after exposure to 3% oxygen for 12 or 24 h of the mRNA levels of the ␣ 1C , ␣ 1B , and ␣ 1A channel subunits that form, respectively, the L-, N-, and P/Q-types of HVA channels previously described in PC12 cells (28,29). Comparison of the threshold cycles of the PCR reveals that the amounts of the three mRNAs are slightly but not significantly increased after 12 or 24 h of hypoxia.…”

Section: Fig 1 Expression Of T-type Ca 2؉ Channels In Pc12 Cellsmentioning

confidence: 99%

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Induction of T-type Calcium Channel Gene Expression by Chronic Hypoxia

Toro

Levitsky

López‐Barneo

et al. 2003

Journal of Biological Chemistry

108

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Cellular responses to hypoxia can be acute or chronic. Acute responses mainly depend on oxygen-sensitive ion channels, whereas chronic responses rely on the hypoxia-inducible transcription factors (HIFs), which upregulate the expression of enzymes, transporters, and growth factors. It is unknown whether the expression of genes coding for ion channels is also influenced by hypoxia. We report here that the ␣ 1H gene of T-type voltage-gated calcium channels is highly induced by lowering oxygen tension in PC12 cells. Accumulation of ␣ 1H mRNA in response to hypoxia is time-and dose-dependent and paralleled by an increase in the density of Ttype calcium channel current recorded in patch clamped cells. HIF appears to be involved in the response to hypoxia, since cobalt chloride, desferrioxamine, and dimethyloxalylglycine, compounds that mimic HIF-regulated gene expression, replicate the hypoxic effect. Moreover, functional inhibition of HIF-2␣ protein accumulation using antisense HIF-2␣ oligonucleotides reverses the effect of hypoxia on T-type Ca 2؉ channel expression. Importantly, regulation by oxygen tension is specific for T-type calcium channels, since it is not observed with the L-, N-, and P/Q-channel types. These findings show for the first time that hypoxia induces an ion channel gene via a HIF-dependent mechanism and define a new role for the T-type calcium channels as regulators of cellular excitability and calcium influx under chronic hypoxia.Maintaining optimal oxygen homeostasis is of paramount importance for cells. Reductions of oxygen supply trigger cell adaptive responses that minimize the deleterious effects of hypoxia. Cellular responses to hypoxia can be acute, occurring over a time scale of seconds or minutes, or chronic, with time courses of hours to days (1-5). The major effectors of the acute cellular responses to hypoxia are oxygen-sensitive ion channels. These channels mediate the fast adaptive changes in cell excitability, contractility, and secretory activity that occur in response to low ambient oxygen tension (PO 2 ) (1, 5). On the other hand, chronic cellular responses to hypoxia, studied in great detail in the past few years, are mediated by ubiquitously expressed hypoxia-inducible transcription factors (HIF-1␣ 1 and isoforms). Stabilization and transcriptional activity of HIF depend on oxygen-regulated hydroxylases (6 -8). Hypoxia-inducible factors regulate the expression of a wide repertoire of oxygen-sensitive genes with roles in diverse cellular functions such as angiogenesis, red blood cell production, glucose and energy metabolism, apoptosis, and cell proliferation (1-5).Despite progress in the understanding of the role of ion channels and gene expression in the cellular responses to hypoxia, long term regulation of ion channel expression by maintained low PO 2 is poorly known. There are previous reports showing that prolonged hypoxia down-regulates various voltage-gated K ϩ (Kv) channel genes in pulmonary artery smooth muscle cells (9), and the opposite has been observed with the ...

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Section: Identification Of T-type Ca 2ϩ Channels In Pc12 Cells-pc12supporting

confidence: 65%

Section: Identification Of T-type Ca 2ϩ Channels In Pc12 Cells-pc12mentioning

confidence: 98%

Section: Fig 1 Expression Of T-type Ca 2؉ Channels In Pc12 Cellsmentioning

confidence: 99%

See 1 more Smart Citation

Induction of T-type Calcium Channel Gene Expression by Chronic Hypoxia

Toro

Levitsky

López‐Barneo

et al. 2003

Journal of Biological Chemistry

108

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“…NGF-differentiated PC12 cells have been demonstrated to possess L-type (dihydropyridine sensitive) and N-type (ω-conotoxin-GIVa sensitive) voltage-dependent Ca 2+ channels [21,22,27,28]. D 2 receptor activation has been shown to block various calcium channels [29][30][31][32].…”

Section: A Pertussis Toxin Sensitive and Voltage-dependent Calcium Chmentioning

confidence: 99%

Mechanism of dopamine mediated inhibition of neuropeptide Y release from pheochromocytoma cells (PC12 cells)

Gui-Hua¹,

Gardner²,

Westfall³

2007

Biochemical Pharmacology

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In rat pheochromocytoma (PC-12) cells the dopamine D 2 receptor agonists apomorphine (APO) and n-propylnorapomorphine (NPA) produced a concentration dependent inhibition of K + -evoked neuropeptide Y release (NPY-ir). The effect of APO was blocked by the dopamine D 2 -receptor antagonist, eticlopride, but not the D 1 /D 3 or the D 4 /D 2 antagonists, SCH23390 or clozapine, respectively. The D 1 /D 5 receptor agonist, SKF38393 or the D 3 agonists PD128907 and 7-OH DPAT had no effect. Selective N and L-type voltage gated Ca 2+ channel blockers, ω-Conotoxin GVIa (CtxGVIa) and nifedipine, respectively, produced a concentration dependent inhibition of NPY-ir release but were not additive with APO. The Ca 2+ /calmodulin-dependent protein kinase (CaM kinase) II inhibitor KN-62 produced a concentration-dependent inhibition of NPY-ir release but the combination of KN-62 and APO produced no further inhibition. PMA-mediated protein kinase C stimulation significantly increased both basal and K + -evoked release of NPY-ir, and in the presence of PMA APO had no inhibitory effect. The PKC antagonist, chelerythrine, inhibited K + -evoked NPYir release but was not additive with APO. Neither forskolin-mediated adenylate cyclase activation and the active cAMP analog Sp-cAMPS, nor the adenylate cyclase inhibitor SQ 22536, and the competitive inhibitor of cAMP-dependent protein kinases Rp-cAMPS, had any significant effect on K + -evoked NPY-ir release. This suggests the inhibitory effect of APO on K + -evoked release of NPYir from PC 12 cells is most likely mediated through activation of dopamine D 2 receptors leading to direct inhibition of N and L-type voltage gated Ca 2+ channels, or indirect inhibition of PKC, both of which would reduce [Ca 2+ ] i and inactivate CaM kinase.

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“…8A]. According to previous studies (15)(16)(17), we found that the whole-cell Ca 2ϩ currents in naïve cells were comprised of low-voltage activated (LVA) and high voltage activated (HVA) conductances (Fig. 1 A).…”

Section: Il1rapl1 Induces a Specific Reduction In Amplitude Of High-vmentioning

confidence: 99%

IL1-receptor accessory protein-like 1 (IL1RAPL1), a protein involved in cognitive functions, regulates N-type Ca ²⁺ -channel and neurite elongation

Gambino

Pavlowsky

Béglé

et al. 2007

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

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. The functional relevance of the interaction between IL1RAPL1 and NCS-1 was also suggested by the reduction of neurite elongation observed in nerve growth factor (NGF)-treated IL1RAPL1 cells, a phenotype rescued by NCS-1 inactivation. Because both proteins are highly expressed in neurons, these results suggest that IL1RAPL1-related mental retardation could result from a disruption of N-VGCC and/or NCS-1-dependent synaptic and neuronal activities.PC12 cells ͉ neuronal calcium sensor-1 ͉ X-linked mental retardation ͉ exocytosis C ognitive impairment or mental retardation (MR) affects Ϸ2% of the population, leading to moderate (IQ Ͻ70) up to severe (IQ Ͻ50) handicap. The underlying causes are extremely heterogeneous, including genetic causes, many of which are X-linked (XLMR) (1, 2). Null mutations in the IL1-receptor accessory protein-like 1 gene (IL1RAPL1) [National Center for Biotechnology Information (NCBI) accession no. NM 014271.2] have been involved in a nonsyndromic form of XLMR (3). IL1RAPL1 and the closely related protein IL1RAPL2 (NCBI accession no. NM 017416) belong to a previously unrecognized class of the interleukin-1/toll receptor family characterized by the presence of a 150-aa C terminus domain with unknown function (3, 4). IL1RAPL1 and IL1RAPL2 have specific, but not redundant, temporal and spatial expression pattern in the brain, Il1rapl1, the mouse homologue of IL1RAPL1, being specifically expressed in adult brain structures that are known to be involved in the hippocampal memory system (3).Most of physiological and biological properties of IL1RAPL proteins remain largely unknown. Recent studies have demonstrated that expression of IL1RAPL1 in PC12 cells leads to a profound inhibition of ATP-induced growth hormone (GH) release (4). The underlying cellular pathways remain to be elucidated; however, IL1RAPL1 has been shown to interact by way of its 150-aa C-terminal domain with the neuronal calcium sensor-1 protein (NCS-1), a protein widely expressed in neurons (5) and the related chromaffin and PC12 cells (6).NCS-1 belongs to a large Ca 2ϩ -binding protein family (7) implicated in the regulation of Ca 2ϩ -dependent exocytosis (6) through its activation of PI 4 kinase and PIP 2 formation (8-10). Moreover, NCS-1 modulates Ca 2ϩ channels trafficking and activity in various cellular models (11, 12) and has effects on synaptic transmission by way of activity-dependent facilitation of P/Q-type calcium currents at presynaptic nerve terminals (13). Finally, at the behavioral level, NCS-1 appears also to be involved in associative learning and memory (14).Here, we focus on IL1RAPL1 functions by studying the physiological impact of IL1RAPL1/NCS-1 interaction in PC12 cells, a well known model of both nerve growth factor (NGF)-induced neuronal differentiation and Ca 2ϩ -dependent exocytosis. We show that expression of IL1RAPL1 in PC12 cells, which do not normally express the IL1RAPL1 protein, mediates, through IL1RAPL1/NSC-1 interaction, a down-regulation of N-type voltage-gated calcium channel (N-VGCC) ac...

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Differential expression by nerve growth factor of two types of Ca2+ channels in rat phaeochromocytoma cell lines.

Cited by 149 publications

References 36 publications

Induction of T-type Calcium Channel Gene Expression by Chronic Hypoxia

Induction of T-type Calcium Channel Gene Expression by Chronic Hypoxia

Mechanism of dopamine mediated inhibition of neuropeptide Y release from pheochromocytoma cells (PC12 cells)

IL1-receptor accessory protein-like 1 (IL1RAPL1), a protein involved in cognitive functions, regulates N-type Ca ²⁺ -channel and neurite elongation

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Differential expression by nerve growth factor of two types of Ca2+ channels in rat phaeochromocytoma cell lines.

Cited by 149 publications

References 36 publications

Induction of T-type Calcium Channel Gene Expression by Chronic Hypoxia

Induction of T-type Calcium Channel Gene Expression by Chronic Hypoxia

Mechanism of dopamine mediated inhibition of neuropeptide Y release from pheochromocytoma cells (PC12 cells)

IL1-receptor accessory protein-like 1 (IL1RAPL1), a protein involved in cognitive functions, regulates N-type Ca 2+ -channel and neurite elongation

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Product

Resources

About

IL1-receptor accessory protein-like 1 (IL1RAPL1), a protein involved in cognitive functions, regulates N-type Ca ²⁺ -channel and neurite elongation