Erythroid involvement in CD36 deficiency

Objective. The CD36 molecule is expressed in platelets, monocytes, erythrob lasts, and other different tissues. The two types of platelet CD36 deficien cy, types I and II, are associated with the absence and presence of CD36 on monocytes, respectively. To clarify the involvement of the erythroid linea ge in CD36 deficiency, we investigated the phenotype and RNA expression of CD36. Materials and Methods. CD36 expression was examined in 296 patients with se veral cardiovascular diseases in our outpatient clinic. There were 12 patie nts with type I deficiency and 16 with type II CD36 deficiency. A bone marr ow 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 seq uences 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 pat ients with type I deficiency. CD36 was present in erythroblasts from three of the four with type II deficiency, suggesting that their abnormality is r estricted to platelets (type IIa). CD36 was unexpectedly absent from erythr oblasts of a single type II patient (type IIb). CD36-specific mRNA was iden tified in BFU-E from each of two normals, six type I, and six type II patie nts, 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 C D36-dericient individuals and the existence of a basic principle mechanism of type II, such as glycosylation abnormality. (C) 2001 International Socie ty for Experimental Hematology. Published by Elsevier Science Inc.