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Decreased expression of phospholipase C-beta 2 isozyme in human platelets with impaired function
Author(s): Lee SB, Rao AK, Lee KH, Yang X, Bae YS, Rhee SG
Source: BLOOD    Volume: 88    Issue: 5    Pages: 1684-1691    Published: SEP 1 1996  
Times Cited: 56     References: 29     
Abstract: Platelets from a patient with a mild inherited bleeding disorder and abnormal platelet aggregation and secretion show reduced generation of inositol 1,4,5-trisphosphate, mobilization of intracellular Ca2+, and phosphorylation of pleckstrin in response to several G protein mediated agonists, suggesting a possible defect at the level of phospholipase C (PLC) activation (see accompanying report), A procedure was developed that allows quantitation of platelet PLC isozymes. After fractionation of platelet extracts by high-performance liquid chromatography, 7 out of 10 known PLC isoforms were detected by immunoblot analysis. The amount of these isoforms in normal platelets decreased in the order PLC-gamma 2 > PLC-beta 2 > PLC-beta 3 > PLC-beta 1 > PLC-gamma 1 > PLC-delta 1 > PLC-beta 4. Compared with normal platelets, platelets from the patient contained approximately one-third the amount of PLC-beta 2, whereas PLC-beta 4 was increased threefold, These results suggest that the impaired platelet function in the patient in response to multiple G protein mediated agonists is attributable to a deficiency of PLC-beta 2. They document for the first time a specific PLC isozyme deficiency in human platelets and provide an unique opportunity to understand the role of different PLC isozymes in normal platelet function. (C) 1996 by The American Society of Hematology.
Document Type: Article
Language: English
Addresses:
1. NHLBI, LAB CELL SIGNALING, NIH, BETHESDA, MD 20892 USA
2. TEMPLE UNIV, SCH MED, SOL SHERRY THROMBOSIS RES CTR, PHILADELPHIA, PA 19122 USA
3. TEMPLE UNIV, SCH MED, DEPT MED, PHILADELPHIA, PA 19122 USA
Publisher: W B SAUNDERS CO, INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399
Subject Category: Hematology
IDS Number: VE234
ISSN: 0006-4971
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