title: Erythroid involvement in CD36 deficiency.
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 of CD36.
  
  
  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 three of 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 mRNA in a patient with type IIa and another with type IIb showed homozygous wild alleles.
  
  
  CONCLUSIONS
  The findings provide evidence for further heterogeneity among CD36-deficient individuals and the existence of a basic principle mechanism of type II, such as glycosylation abnormality.
authors.affiliation: First Department of Internal Medicine, Niigata University, Niigata City, Japan. tobaken@med.niigata-u.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Toba
authors.forename: H
authors.initials: H
authors.lastname: Hanawa
authors.forename: K
authors.initials: K
authors.lastname: Watanabe
authors.forename: I
authors.initials: I
authors.lastname: Fuse
authors.forename: M
authors.initials: M
authors.lastname: Masuko
authors.forename: S
authors.initials: S
authors.lastname: Miyajima
authors.forename: M
authors.initials: M
authors.lastname: Takahashi
authors.forename: M
authors.initials: M
authors.lastname: Sakaue
authors.forename: T
authors.initials: T
authors.lastname: Abo
authors.forename: Y
authors.initials: Y
authors.lastname: Aizawa
mesh_terms: D000787:Angina Pectoris / Q000235:genetics; D015703:Antigens, CD / Q000235:genetics; D018955:CD36 Antigens / Q000235:genetics*; D002311:Cardiomyopathy, Dilated / Q000235:genetics; D002312:Cardiomyopathy, Hypertrophic / Q000235:genetics; D002318:Cardiovascular Diseases / Q000235:genetics*; D002478:Cells, Cultured; D002874:Chromosome Mapping; D002897:Chromosomes, Human, Pair 7; D003114:Colony-Forming Units Assay; D005091:Exons; D005434:Flow Cytometry; D006410:Hematopoiesis / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D009000:Monocytes / Q000502:physiology*; D014176:Protein Biosynthesis; D012016:Reference Values; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D015703:Antigens, CD; D018955:CD36 Antigens; D007074:Immunoglobulin G