Capacitative calcium entry is involved in steroidogenesis in bovine adrenocortical fasciculata cells

Ebisawa, Takanori; Kondo, Isamu; Masaki, Eiji; Hori, Seiji; Kawamura, Masahiro

doi:10.1677/joe.0.1670473

Cited by 9 publications

(5 citation statements)

References 15 publications

(22 reference statements)

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“…The main finding of the present work was that STIM1, which plays an essential role in transmitting a decrease in store Ca 2ϩ contents to the plasma membrane, was not detected in rat AM cells at the mRNA and protein levels. On the other hand, STIM1 was expressed in adrenal cortex cells, where SOC has been implicated in the production of steroid hormones (8,44). The lack of STIM1 expression strongly suggests that SOC is absent in the rat AM cells.…”

Section: Discussionmentioning

confidence: 98%

Ca²⁺ pathway involved in the refilling of store sites in rat adrenal medullary cells

Matsuoka

Harada²,

Ikeda³

et al. 2009

American Journal of Physiology-Cell Physiology

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It has been suggested that store-operated Ca(2+) entry (SOC) facilitates catecholamine secretion and synthesis in bovine adrenal medullary (AM) cells. However, there has been no experimental result clearly showing that cation channel activity is enhanced by store Ca(2+) depletion. Thus the present experiments were undertaken to address the issue of whether rat AM cells have SOC channels. Inhibition of the sarco(endo)plasmic reticulum Ca(2+) (SERCA) pump resulted in a sustained increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) in rat AM cells. This increase was completely suppressed by 2 mM Ni(2+) but not by 100 muM D600. A bath application of Ni(2+), but not D600, produced an outward current at -60 mV in rat AM cells, whereas exposure to a SERCA pump inhibitor did not affect either the whole cell current level or the Ni(2+)-induced outward current. The refilling of intracellular store sites was suppressed by the addition of Ni(2+) to the perfusate. RT-PCR revealed that transcripts for transient receptor potential channels 1 (TRPC1) and 5 (TRPC5) were present in rat adrenal medullas. Immunocytochemistry showed that TRPC1 channels, which have been implicated in SOC in certain types of cells, were mainly localized in the endoplasmic reticulum (ER) and not in the plasma membrane, and that STIM1, a Ca(2+) sensor in the ER, was not expressed in rat AM cells. On the basis of these results, we conclude that rat AM cells lack the SOC mechanism.

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Section: Discussionmentioning

confidence: 98%

Ca²⁺ pathway involved in the refilling of store sites in rat adrenal medullary cells

Matsuoka

Harada²,

Ikeda³

et al. 2009

American Journal of Physiology-Cell Physiology

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“…1–4) which could explain the toxicity in CsA‐treated rat heart (Goldberg et al, 1989). It has been reported that voltage‐dependent L‐Type Ca 2+ ‐channel are regulated by glucocorticoids (Braun et al, 1995; Ebisawa et al, 2000). In our experimental conditions, HY inhibited CsA‐induced calcium increase as well as MDA production.…”

Section: Discussionmentioning

confidence: 99%

Hydrocortisone has a protective effect on CyclosporinA‐induced cardiotoxicity

Florio

Ciarcia

Crispino

et al. 2003

Journal Cellular Physiology

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CyclosporinA (CsA) is an immunosuppressive drug which induces severe adverse effects such as cardiotoxicity and nephrotoxicity. In several therapeutic protocols CsA is used in association with corticosteroids to obtain better therapeutic results. Recently, our studies showed that CsA increases blood pressure while inhibit Nitric Oxide (NO) production in vivo. In this study we evaluated in rat cardiomyocytes the effects of CsA, used alone or in association with Hydrocortisone (HY), on intracellular calcium concentration, NO production and lipid peroxidation (MDA level). Our results demonstrated that CsA increased intracellular calcium and such effect was dose-dependent. HY used alone, slightly decreased intracellular calcium, while dramatically reduced CsA-induced calcium fluxes. CsA (3.2 microM) increased lipid peroxidation and this effect was blunted by HY. Both CsA and HY inhibited NO production in rat cardiomyocytes acting on this pathway synergically. Our results demonstrated that in rat cardiomyocytes, CsA toxicity is due to a calcium overload, which in turn induce lipid peroxidation and determines oxidative stress-induced cell injury. Treatment with HY effectively inhibits CsA-induced toxicity, decreasing lipid peroxidation as well as calcium intracellular concentration. Our findings seem to suggest that glucocorticoids may be effective in reducing CsA-induced cardiotoxicity at concentrations which are consistent with current therapeutic doses.

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“…The isolated cells were cultured in Ham's F-10 medium supplemented with 5% fetal calf serum, 10% newborn calf serum, 2.5% horse serum, and antibiotics on a coverslip coated with collagen (16,17). Three-day primary cultured monolayer cells were used for the experiments.…”

Section: Primary Culture Of Bafcsmentioning

confidence: 99%

“…] i was monitored as described by Ebisawa et al (17). Briefly, BAFCs on a coverslip were loaded with 5 m M fura 2 / AM in Krebs-Ringer HEPES buffer (123.4 mM NaCl, 6 mM KCl, 1.2 mM KH 2 PO 4 , 1.2 mM MgSO 4 , 1.2 mM CaCl 2 , 2 mg / ml glucose, 2 mg / ml BSA, 10 mM HEPES, pH 7.4) supplemented with 0.02% cremophor EL for 90 min at 37°C.…”

Section: +mentioning

confidence: 99%

Integrity of Actin-Network Is Involved in Uridine 5'-Triphosphate Evoked Store-Operated Ca2+ Entry in Bovine Adrenocortical Fasciculata Cells

et al. 2003

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Abstract. Store-operated Ca 2+ entry channels (SOCs) play an important role in the regulation of diverse non-excitable cell functions. However, the precise mechanism of SOCs activation is still controversial. Uridine 5'-triphosphate (UTP) was shown to induce Ca 2+ entry in a dihydropyridines-insensitive manner and accelerated steroidogenesis in bovine adrenocortical fasciculata cells (BAFCs) via the Gq / 11 protein-coupled P2Y 2 receptor. Therefore we investigated whether UTP is involved in SOCs activation and the mechanism of UTP-induced SOCs activation. Fura 2-loaded BAFCs were used for the measurement of intracellular concentration of Ca ), and the effect of UTP was also attenuated by a phospholipase C inhibitor (U73122). These results indicate that UTP activates SOCs in BAFCs. The increase in [Ca 2+ ] i by UTP was attenuated by ML-9, a myosin-light chain kinase inhibitor, and calmodulin inhibitors, W-7 and E6 berbamine, in a concentration-dependent manner. These reagents depolymerized actin filaments with rhodamine staining in BAFCs. Cytochalasin D also inhibited UTP-activated SOCs and depolymerized actin filaments. From these results, we proposed that calcium / calmodulin dependent myosin-light chain kinase is involved in the mobilization of actin filaments and the integrity of actin-network plays an important role in UTP-induced SOCs activation in BAFCs.

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Capacitative calcium entry is involved in steroidogenesis in bovine adrenocortical fasciculata cells

Abstract: Abstract

Cited by 9 publications

References 15 publications

Ca²⁺ pathway involved in the refilling of store sites in rat adrenal medullary cells

Ca²⁺ pathway involved in the refilling of store sites in rat adrenal medullary cells

Hydrocortisone has a protective effect on CyclosporinA‐induced cardiotoxicity

Integrity of Actin-Network Is Involved in Uridine 5'-Triphosphate Evoked Store-Operated Ca2+ Entry in Bovine Adrenocortical Fasciculata Cells

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Capacitative calcium entry is involved in steroidogenesis in bovine adrenocortical fasciculata cells

Abstract: Abstract

Cited by 9 publications

References 15 publications

Ca2+ pathway involved in the refilling of store sites in rat adrenal medullary cells

Ca2+ pathway involved in the refilling of store sites in rat adrenal medullary cells

Hydrocortisone has a protective effect on CyclosporinA‐induced cardiotoxicity

Integrity of Actin-Network Is Involved in Uridine 5'-Triphosphate Evoked Store-Operated Ca2+ Entry in Bovine Adrenocortical Fasciculata Cells

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Ca²⁺ pathway involved in the refilling of store sites in rat adrenal medullary cells

Ca²⁺ pathway involved in the refilling of store sites in rat adrenal medullary cells