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P2Y receptors contr...
P2Y receptors contribute to ATP-induced increases in intracellular calcium in differentiated but not undifferentiated PC12 cells
- Artikel/kapitelEngelska2000
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LIBRIS-ID:oai:lup.lub.lu.se:252ee673-3dbb-49c6-88cb-c2711345b51a
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https://lup.lub.lu.se/record/1117336URI
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https://doi.org/10.1016/S0028-3908(99)00141-0DOI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:1940035URI
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Språk:engelska
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Sammanfattning på:engelska
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Ämneskategori:art swepub-publicationtype
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Ämneskategori:ref swepub-contenttype
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ATP-induced Ca2+ transients were examined in individual PC12 cells of a well defined clone, before and after treatment with nerve growth factor (NGF) to induce a neurone-like phenotype. Using reverse transcriptase PCR these cells were found to express mRNA for several P2 receptors. In undifferentiated cells the ATP-induced Ca2+ response was entirely dependent on Ca2+ influx, could not be mimicked by UTP, alpha,beta-methylene ATP or dibenzoyl ATP or be blocked by pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS). ATP had no significant effect on levels of cyclic AMP or inositol 1,4,5-trisphosphate (InsP3). These results suggest that in undifferentiated PC12 cells ATP mainly acts on a P2X receptor, possibly the P2X4 subtype. After treatment with NGF for 7 days the ATP response was increased and partially sensitive to PPADS. A component of the ATP-induced Ca2+ increase was due to mobilisation of intracellular Ca2+ stores and another to capacitative Ca2+ entry. UTP caused an increase in intracellular Ca2+, and InsP3 formation could be stimulated by ATP and UTP. ATP also caused a small increase in cyclic AMP, but this was abolished in the presence of indomethacin. Thus, after NGF treatment ATP acts partially via a P2Y receptor, possibly the P2Y2 subtype.
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Biuppslag (personer, institutioner, konferenser, titlar ...)
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Filipeanu, C M
(författare)
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Irenius, E
(författare)
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Kull, BKarolinska Institutet
(författare)
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Clementi, E
(författare)
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Allgaier, C
(författare)
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Erlinge, DavidLund University,Lunds universitet,Kardiologi,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Cardiology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)kard-der
(författare)
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Fredholm, B BKarolinska Institutet
(författare)
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Catalin, CM
(författare)
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Karolinska InstitutetKardiologi
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Neuropharmacology39:3, s. 482-4961873-70640028-3908
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