@article{oai:niigata-u.repo.nii.ac.jp:00001655,
 author = {Toba, Ken and Hanawa, Haruo and Watanabe, Kenichi and Fuse, Ichiro and Masuko, Masayoshi and Miyajima, Seiichi and Takahashi, Masuhiro and Sakaue, Minori and Abo, Toru and Aizawa, Yoshifusa},
 issue = {10},
 journal = {Experimental Hematology, Experimental Hematology},
 month = {Oct},
 note = {Objective. The CD36 molecule is expressed in platelets, monocytes, erythroblasts, and other different tissues. There are 2 types of platelet CD36 deficiency; types I and II, 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 of CD36. Materials and Methods. CD36 expression was examined in 296 patients with several cardiovascular diseases in our outpatient clinic. Of them, there were 12 patients with type I and 16 with type II CD36 deficiency. A bone marrow sample was examined in 5 type I and 4 type II patients. The expression of CD36 mRNA was examined in BFU-e. The sequences of RT-PCR products of the CD36 mRNA from monocytes were examined. Results. CD36 was deficient in erythroblasts from all the 5 patients with type I as expected. CD36 was present in erythroblasts from 3 of the 4 with type II, 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-speciflc mRNA was identified in BFU-e from each of 2 normals, 6 type I and 6 type II including type IIb. The sequences of RT-PCR products of the CD36 mRNA in a patient with type IIa and another with type IIb showed homozygous wild alleles. Conclusion. The findings provide evidence for further heterogeneity among CD36 deficient individuals, and existence of basic principle mechanism of type II, such as glycosylation abnormality.},
 pages = {1194--1200},
 title = {Erythroid Involvement in CD36 Deficiency},
 volume = {29},
 year = {2001}
}