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Titolo:
Ca2+-dependent exocytosis of L-glutamate by alpha TC6, clonal mouse pancreatic alpha-cells
Autore:
Yamada, H; Otsuka, M; Hayashi, M; Nakatsuka, S; Hamaguchi, K; Yamamoto, A; Moriyama, Y;
Indirizzi:
Okayama Univ, Fac Pharmaceut Sci, Dept Biochem, Okayama 7008530, Japan Okayama Univ Okayama Japan 7008530 Dept Biochem, Okayama 7008530, Japan Oita Med Univ, Fac Med, Oita, Japan Oita Med Univ Oita JapanOita Med Univ, Fac Med, Oita, Japan Kanazawa Med Univ, Dept Physiol, Moriguchi, Osaka, Japan Kanazawa Med Univ Moriguchi Osaka Japan Physiol, Moriguchi, Osaka, Japan Japan Sci & Technol Corp, CREST, Osaka, Japan Japan Sci & Technol Corp Osaka Japan Technol Corp, CREST, Osaka, Japan
Titolo Testata:
DIABETES
fascicolo: 5, volume: 50, anno: 2001,
pagine: 1012 - 1020
SICI:
0012-1797(200105)50:5<1012:CEOLBA>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
GAMMA-AMINOBUTYRIC-ACID; MICROVESICLE-MEDIATED EXOCYTOSIS; VESICULAR MONOAMINE TRANSPORTER; SYNAPTIC-LIKE MICROVESICLES; EXCITATORY AMINO-ACIDS; OMEGA-AGA-IVA; RAT PINEALOCYTES; CHEMICAL TRANSDUCTION; GLUCAGON-SECRETION; INSULIN-SECRETION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Moriyama, Y Okayama Univ, Fac Pharmaceut Sci, Dept Biochem, 2-5-1 Shikata Cho, Okayama7008530, Japan Okayama Univ 2-5-1 Shikata Cho Okayama Japan 7008530 0, Japan
Citazione:
H. Yamada et al., "Ca2+-dependent exocytosis of L-glutamate by alpha TC6, clonal mouse pancreatic alpha-cells", DIABETES, 50(5), 2001, pp. 1012-1020

Abstract

Pancreatic islet cells express receptors and transporters for L-glutamate and are thus believed to nse L-glutamate as an intercellular signaling molecule. However, the mechanism by which L-glutamate appears in the islets is unknown. In the present study, me investigated whether L-glutamate is secreted through exocytosis by alpha TC6 cells (clonal mouse pancreatic or-cells). An appreciable amount of L-glutamate mas released from cultured cells after the addition of KCl or A23181 in the presence of Ca2+ and 10 mmol/l glucose in the medium. The KCl-induced glutamate release was significantly reduced when assayed in the absence of Ca2+ or when the cells were pretreated with EGTA-AM. The KCl-induced Ca2+-dependent glutamate release was inhibited similar to 40% by voltage-gated Ca2+ channel blockers, such as nifedipineat 20 mu mol/l. The degree of KCl-induced Ca2+-dependent glutamate releasewas correlated with an increase in intracellular [Ca2+], as monitored by fura-a fluorescence. Botulinum neurotoxin type E inhibited 55% of the KCl-induced Ca2+ dependent glutamate release, followed by specific cleavage of 25kDa synaptosomal-associated protein. Furthermore, bafilomycin A,, a specific inhibitor of vacuolar Hf-ATPase, inhibited 40% of the KCl-induced Ca2+-dependent glutamate release. Immunoelectronmicroscopy with antibodies against synaptophysin, a marker for neuronal synaptic vesicles and endocrine synaptic-like microvesicles, revealed a large number of synaptophysin-positive clear vesicles in cells. Digitonin-permeabilized cells took up L-glutamate only in the presence of MgATP, which is sensitive to bafilomycin A(1) or 3,5-di-tert-butyl-4-hydroxybenzglidene-malononitrile (a proton conductor) butinsensitive to either oligomycin or vanadate. From these results, it was concluded that alpha TC6 cells accumulate L-glutamate in the synaptophysin-containing vesicles in an ATP-dependent manner and secrete it through a Ca2+-dependent exocytic mechanism. The Ca2+-dependent glutamate release was also triggered when cells were transferred in the medium containing 1 mmol/l glucose, suggesting that low glucose treatment stimulates the release of glutamate. Our results are consistent with the idea that L-glutamate is secreted by alpha -cells through Ca2+-dependent regulated exocytosis.

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Documento generato il 05/04/20 alle ore 02:29:27