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Titolo:
Erythroid involvement in CD36 deficiency
Autore:
Toba, K; Hanawa, H; Watanabe, K; Fuse, I; Masuko, M; Miyajima, S; Takahashi, M; Sakaue, M; Abo, T; Aizawa, Y;
Indirizzi:
Niigata Univ, Sch Med, Dept Internal Med 1, Niigata 9518510, Japan NiigataUniv Niigata Japan 9518510 nternal Med 1, Niigata 9518510, Japan Niigata Univ, Sch Med, Dept Immunol, Niigata 9518510, Japan Niigata Univ Niigata Japan 9518510 Dept Immunol, Niigata 9518510, Japan Niigata Univ, Fac Med, Sch Hlth Sci, Niigata 9518510, Japan Niigata Univ Niigata Japan 9518510 Sch Hlth Sci, Niigata 9518510, Japan Niigata Coll Pharm, Dept Clin Pharmacol, Niigata 95021, Japan Niigata CollPharm Niigata Japan 95021 n Pharmacol, Niigata 95021, Japan Tsubame Rosai Hosp, Niigata, Japan Tsubame Rosai Hosp Niigata JapanTsubame Rosai Hosp, Niigata, Japan
Titolo Testata:
EXPERIMENTAL HEMATOLOGY
fascicolo: 10, volume: 29, anno: 2001,
pagine: 1194 - 1200
SICI:
0301-472X(200110)29:10<1194:EIICD>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLYCOPROTEIN-IV CD36; CHAIN FATTY-ACIDS; HYPERTROPHIC CARDIOMYOPATHY; ENDOTHELIAL-CELLS; MEMBRANE-PROTEIN; EPITHELIAL-CELLS; PLATELET; EXPRESSION; RECEPTOR; GENE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Toba, K Niigata Univ, Sch Med, Dept Internal Med 1, Asahimachi Dori 1, Niigata 9518510, Japan Niigata Univ Asahimachi Dori 1 Niigata Japan 9518510 18510, Japan
Citazione:
K. Toba et al., "Erythroid involvement in CD36 deficiency", EXP HEMATOL, 29(10), 2001, pp. 1194-1200

Abstract

Objective. The CD36 molecule is expressed in platelets, monocytes, erythroblasts, and other different tissues. The two types of platelet CD36 deficiency, types I and II, are associated with the absence and presence of CD36 on monocytes, respectively. To clarify the involvement of the erythroid lineage in CD36 deficiency, we investigated the phenotype and RNA expression ofCD36. Materials and Methods. CD36 expression was examined in 296 patients with several cardiovascular diseases in our outpatient clinic. There were 12 patients with type I deficiency and 16 with type II CD36 deficiency. A bone marrow sample was examined in five type I and four type II patients. Expression of CD36 mRNA was examined in burst-forming unit-erythroid (BFU-E). The sequences of reverse transcriptase polymerase chain reaction (RT-PCR) products of the CD36 mRNA from monocytes were examined. Results. As expected, CD36 was deficient in erythroblasts from all five patients with type I deficiency. CD36 was present in erythroblasts from threeof the four with type II deficiency, suggesting that their abnormality is restricted to platelets (type IIa). CD36 was unexpectedly absent from erythroblasts of a single type II patient (type IIb). CD36-specific mRNA was identified in BFU-E from each of two normals, six type I, and six type II patients, including type IIb. The sequences of RT-PCR products of the CD36 mRNAin a patient with type IIa and another with type IIb showed homozygous wild alleles. Conclusion. The findings provide evidence for further heterogeneity among CD36-dericient individuals and the existence of a basic principle mechanismof type II, such as glycosylation abnormality. (C) 2001 International Society for Experimental Hematology. Published by Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 00:47:08