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The polymorphism analysis for CD36 among platelet donors.

Qilu Lyu1,2, Yuwei Lin1,2,3, Yiming Pan1,2

  • 1Clinical Transfusion Research Center, Institute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Chengdu, 610052, Sichuan, China.

Scientific Reports
|April 12, 2024
PubMed
Summary
This summary is machine-generated.

CD36 deficiency involves altered CD36 gene and protein levels. This study identifies prevalent mutations and links RNA alterations to type II deficiency, suggesting soluble CD36 (sCD36) as a potential biomarker.

Keywords:
CD36Platelet donorsPolymorphismsCD36

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Area of Science:

  • Genetics and Molecular Biology
  • Immunology
  • Biochemistry

Background:

  • CD36 deficiency, characterized by defects in CD36 on platelets and/or monocytes, has incompletely understood correlations between molecular and protein expression levels.
  • Investigating these correlations is crucial for understanding the pathophysiology of CD36 deficiency.

Purpose of the Study:

  • To determine the polymorphisms of the CD36 gene, its RNA levels, and CD36 protein expression on platelets and in plasma.
  • To correlate genetic variations with molecular and protein expression changes in CD36 deficiency.

Main Methods:

  • Sanger sequencing for CD36 gene polymorphisms.
  • Bioinformatic analysis using HotMuSiC, CUPSAT, SAAFEC-SEQ, and FoldX.
  • Quantitative PCR (qPCR), flow cytometry, and ELISA for RNA and protein level analysis.

Main Results:

  • Identified c.1228_1239delATTGTGCCTATT as the most frequent mutation (allele frequency 0.0072).
  • Confirmed 5 mutations in the extracellular domain, with four (c.284T>C, c.512A>G, c.572C>T, c.869T>C) predicted to deleteriously impact CD36 protein stability.
  • Observed significantly lower mean fluorescence intensity (MFI) of platelet CD36 expression in mutation carriers and deficient individuals.
  • Found significantly lower soluble CD36 (sCD36) levels in type II deficiency and lower CD36 RNA levels in platelets of type II individuals compared to controls.

Conclusions:

  • RNA level alterations may underlie type II CD36 deficiency.
  • The prevalent mutation c.1228_1239delATTGTGCCTATT was identified in the Kunming cohort.
  • Soluble CD36 (sCD36) shows potential as a biomarker for assessing immune reaction risk in CD36-deficient individuals, warranting further investigation.