Succinate independently stimulates full platelet activation via cAMP and PI3β kinase signaling.

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Fältnamn	Indikatorer	Metadata
000		04933naa a2200445 4500
001		oai:lup.lub.lu.se:25c2944c-e1e6-4892-9781-cbb4b9e6dea6
003		SwePub
008		160401s2011 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://lup.lub.lu.se/record/17565672 URI
024	7	a https://doi.org/10.1111/j.1538-7836.2010.04158.x2 DOI
040		a (SwePub)lu
041		a engb eng
042		9 SwePub
072	7	a art2 swepub-publicationtype
072	7	a ref2 swepub-contenttype
100	1	a Högberg, Carlu Lund University,Lunds universitet,Kardiologi,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Cardiology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)kard-clh
245	1 0	a Succinate independently stimulates full platelet activation via cAMP and PI3β kinase signaling.
264	1	b Elsevier BV,c 2011
520		a Background: The citric cycle intermediate succinate has recently been identified as ligand for the G-protein coupled receptor (GPCR) SUCNR1. We have previously found that this receptor is one of the most expressed GPCRs in human platelets. Objective: The aim of this study was to investigate the role of SUCNR1 in platelet aggregation and to explore the signalling pathways of this receptor in platelets. Methods and Results: Using RT-PCR, we could demonstrate that SUCNR1 is expressed in human platelets at a level corresponding to that of the P2Y(1) receptor. Light transmission aggregation experiments showed a dose-dependent aggregation induced by succinate reaching a maximum response at 0.5mM. The effect of succinate on platelet aggregation was confirmed with flow cytometry showing increased surface expression of activated GPIIb/IIIa, and P-selectin. Intracellular SUCNR1 signalling was found to result in decreased cAMP levels, Akt phosphorylation mediated by PI3Kβ activation and receptor desensitisation. Further, succinate-induced platelet aggregation was demonstrated to depend on Src, generation of thromboxane A(2) and ATP release. The platelet SUCNR1 is subject to desensitization through both homologous and heterologous mechanisms. In addition, the P2Y(12) receptor inhibitor ticagrelor completely prevented platelet aggregation induced by succinate. Conclusions: Our experiments show that succinate induces full aggregation of human platelets via SUCNR1. Succinate-induced platelet aggregation depends on thromboxane A(2) generation, ATP release and P2Y(12) activation.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Kardiologi0 (SwePub)302062 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Cardiac and Cardiovascular Systems0 (SwePub)302062 hsv//eng
653		a GPR91
653		a GPCR
653		a PI3K
653		a platelet
653		a succinate
653		a SUCNR1
700	1	a Gidlöf, Olofu Lund University,Lunds universitet,Kardiologi,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Cardiology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)med-ogf
700	1	a Tan, Chanyuanu Lund University,Lunds universitet,Kardiologi,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Cardiology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)med-cht
700	1	a Svensson, Sivu Lund University,Lunds universitet,Kardiologi,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Cardiology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)kkem-ssv
700	1	a Öhman, Jennyu Lund University,Lunds universitet,Kardiologi,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Cardiology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)mphy-jni
700	1	a Erlinge, Davidu Lund University,Lunds universitet,Kardiologi,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Cardiology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)kard-der
700	1	a Olde, Björnu Lund University,Lunds universitet,Kardiologi,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Cardiology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)mphy-bol
710	2	a Kardiologib Sektion II4 org
773	0	t Journal of Thrombosis and Haemostasisd : Elsevier BVg 9:2, s. 361-372q 9:2<361-372x 1538-7933x 1538-7836
856	4	u http://www.ncbi.nlm.nih.gov/pubmed/21143371?dopt=Abstracty FULLTEXT
856	4	u http://dx.doi.org/10.1111/j.1538-7836.2010.04158.xy FULLTEXT
856	4	u https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/j.1538-7836.2010.04158.x
856	4 8	u https://lup.lub.lu.se/record/1756567
856	4 8	u https://doi.org/10.1111/j.1538-7836.2010.04158.x

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Av författaren/redakt...: Högberg, Carl; Gidlöf, Olof; Tan, Chanyuan; Svensson, Siv; Öhman, Jenny; Erlinge, David; visa fler...; Olde, Björn; visa färre...

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