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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Mao, G. F. Articles by Rao, A. K. Search for Related Content PubMed PubMed Citation Articles by Mao, G. F. Articles by Rao, A. K. Related Collections Hemostasis, Thrombosis, and Vascular Biology Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 February 2002, Vol. 99, No. 3, pp. 905-911 HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Lineage-specific defect in gene expression in human platelet phospholipase C-2 deficiency Guang Fen Mao, Vijender R. Vaidyula, Satya P. Kunapuli, and A. Koneti Rao From the Sol Sherry Thrombosis Research Center, and the Departments of Medicine and Physiology, Temple University School of Medicine, Philadelphia, PA. Phospholipase C (PLC)-2 plays a major role in platelet activation. Previous studies have described a unique patient with impaired receptor-mediated platelet aggregation, secretion, calcium mobilization, and phospholipase C (PLC) activation associated with a selective decrease in platelet PLC-2 isozyme. To identify the mechanisms leading to the defect, platelet RNA from the patient and healthy subjects was subjected to reverse transcription-polymerase chain reaction (RT-PCR) and the products sequenced. The PLC-2 cDNA sequence in the patient showed no abnormalities. Platelet PLC-2 and -actin (internal control) mRNA levels were assessed by RT-PCR; the ratio of PLC-2 to -actin mRNA levels was 0.80 to 0.95 in 4 healthy subjects and 0.28 in the patient. PLC-2 mRNA levels were similarly reduced compared with GPIIb and Gq mRNA levels. PLC-2 and platelet factor 4 mRNA levels were normal. Calcium mobilization was studied in neutrophils upon activation with formyl-Met-Leu-Phe (fMLP), adenosine diphosphate (ADP), platelet-activating factor (PAF), interleukin-8 (IL-8), C5a, and leukotriene B4 (LTB4), and it was normal. Neutrophil elastase secretion upon activation with fMLP, ADP, PAF, IL-8, C5a, and LTB4 was normal, as were neutrophil PLC-2 mRNA and PLC-2 on immunoblotting. Thus, responses to activation, PLC-2 protein, and PLC-2 mRNA are decreased in patient platelets but not in neutrophils, providing evidence for a hitherto undescribed lineage (platelet)-specific defect in PLC-2 gene expression. These studies provide a physiologically relevant model to delineate regulation of PLC-2 gene and its tissue-specific expression. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: G. Mao, S. P. Kunapuli, and A. K. Rao Regulation of Platelet PLC-{beta}2 Expression by NF-{kappa}B: Studies in Human Platelet PLC-{beta}2 Deficiency. Blood (ASH Annual Meeting Abstracts), November 16, 2006; 108(11): 699 - 699. [Abstract] [PDF]

	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020