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Sökning: onr:"swepub:oai:DiVA.org:oru-42401" > A novel role for ph...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005630naa a2200553 4500
001oai:DiVA.org:oru-42401
003SwePub
008150204s2012 | |||||||||||000 ||eng|
009oai:DiVA.org:liu-80685
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-424012 URI
0247 a https://doi.org/10.1016/j.cellsig.2012.04.0182 DOI
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-806852 URI
040 a (SwePub)orud (SwePub)liu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Elvers, Margittau Medizinische Klinik III, Dept. of Cardiology and Cardiovascular Diseases, Eberhard Karls University, Tübingen, Germany4 aut
2451 0a A novel role for phospholipase D as an endogenous negative regulator of platelet sensitivity
264 1a New York, USA :b Elsevier,c 2012
338 a print2 rdacarrier
520 a Platelet aggregation, secretion and thrombus formation play a critical role in primary hemostasis to prevent excessive blood loss. On the other hand, uncontrolled platelet activation leads to pathological thrombus formation resulting in myocardial infarction or stroke. Stimulation of heterotrimeric G-proteins by soluble agonists or immunoreceptor tyrosine based activation motif-coupled receptors that interact with immobilized ligands such as the collagen receptor glycoprotein (GP) VI lead to the activation of phospholipases that cleave membrane phospholipids to generate soluble second messengers. Platelets contain the phospholipases (PL) D1 and D2 which catalyze the hydrolysis of phosphatidylcholine to generate the second messenger phosphatidic acid (PA). The production of PA is abrogated by primary alcohols that have been widely used for the analysis of PLD-mediated processes. However, it is not clear if primary alcohols effectively reduce PA generation or if they induce PLD-independent cellular effects. In the present study we made use of the specific PLD inhibitor 5-fluoro-2-indolyl des-chlorohalopemide (FIPI) and show for the first time, that FIPI enhances platelet dense granule secretion and aggregation of human platelets. Further, FIPI has no effect on cytosolic Ca(2+) activity but needs proper Rho kinase signaling to mediate FIPI-induced effects on platelet activation. Upon FIPI treatment the phosphorylation of the PKC substrate pleckstrin was prominently enhanced suggesting that FIPI affects PKC-mediated secretion and aggregation in platelets. Similar effects of FIPI were observed in platelets from mouse wild-type and Pld1(-/-) mice pointing to a new role for PLD2 as a negative regulator of platelet sensitivity.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Farmakologi och toxikologi0 (SwePub)301022 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Pharmacology and Toxicology0 (SwePub)301022 hsv//eng
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Cell- och molekylärbiologi0 (SwePub)301082 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Cell and Molecular Biology0 (SwePub)301082 hsv//eng
653 a PLD
653 a platelets
653 a secretion
653 a aggregation
653 a regulation
653 a MEDICINE
7001 a Grenegård, Magnus,d 1963-u Linköpings universitet,Farmakologi,Hälsouniversitetet4 aut0 (Swepub:liu)maggr06
7001 a Khoshjabinzadeh, Haniehu Linköpings universitet,Klinisk kemi,Hälsouniversitetet4 aut
7001 a Münzer, Patricku Department of Physiology, Eberhard Karls University, Tübingen, Germany4 aut
7001 a Borst, Oliveru Medizinische Klinik III, Dept. of Cardiology and Cardiovascular Diseases, Eberhard Karls University, Tübingen, Germany; Department of Physiology, Eberhard Karls University, Tübingen, Germany4 aut
7001 a Tian, Huasongu Department of Pathology and Cell Biology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Medical Center, New York, USA,Columbia University, NY 10032 USA4 aut
7001 a Di Paolo, Gilbertu Department of Pathology and Cell Biology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Medical Center, New York, USA,Columbia University, NY 10032 USA4 aut
7001 a Lang, Florianu Department of Physiology, Eberhard Karls University, Tübingen, Germany4 aut
7001 a Gawaz, Meinradu Medizinische Klinik III, Dept. of Cardiology and Cardiovascular Diseases, Eberhard Karls University, Tübingen, Germany4 aut
7001 a Lindahl, Tomasu Östergötlands Läns Landsting,Linköpings universitet,Klinisk kemi,Hälsouniversitetet4 aut0 (Swepub:liu)tomli13
7001 a Fälker, Knutu Linköpings universitet,Institutionen för klinisk och experimentell medicin,Hälsouniversitetet4 aut0 (Swepub:liu)knufa08
7102 a Medizinische Klinik III, Dept. of Cardiology and Cardiovascular Diseases, Eberhard Karls University, Tübingen, Germanyb Farmakologi4 org
7730 t Cellular Signallingd New York, USA : Elsevierg 24:9, s. 1743-52q 24:9<1743-52x 0898-6568x 1873-3913
8564 u http://liu.diva-portal.org/smash/get/diva2:547904/FULLTEXT01
8564 u https://liu.diva-portal.org/smash/get/diva2:547904/FULLTEXT01.pdfx primaryx Raw objecty fulltext:postprint
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-42401
8564 8u https://doi.org/10.1016/j.cellsig.2012.04.018
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-80685

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