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|Title:||microRNA-27a and microRNA-146a SNP in cerebral malaria|
|Authors:||Saw Thu Wah|
University of Tokyo
University of Medical Technology
|Keywords:||Biochemistry, Genetics and Molecular Biology;Medicine|
|Citation:||Molecular Genetics and Genomic Medicine. Vol.7, No.2 (2019)|
|Abstract:||© 2019 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals, Inc. Background: During Plasmodium falciparum infection, microRNA expression alters in brain tissue of mice with cerebral malaria compared to noninfected controls. MicroRNA regulates gene expression post-transcriptionally to influence biological processes. Cerebral malaria pathology caused mainly by the immunological disorder. We hypothesize that single-nucleotide polymorphism in a microRNA influences microRNA biogenesis or target gene recognition and altering susceptibility to cerebral malaria. Methods: We performed a literature search based on immunological mechanism and applied microRNA-related single-nucleotide polymorphisms database to examine candidate microRNA SNPs possibly responsible for cerebral malaria. MicroRNA-27a and microRNA-146a are supposed to involve in cerebral malaria pathology. To assess the relationship of microRNA SNP to cerebral malaria outcome, we performed TaqMan Genotyping Assays in 110 cerebral malaria and 207 uncomplicated malaria cases for three candidate microRNA SNPs (rs895819 of microRNA-27a, rs57095329 and rs2910164 of microRNA-146a). Results: Our study detected no significant difference in genotype and allele frequency of individual microRNA SNPs as well as in haplotypes of microRNA-146a between these two groups of malaria patients in Thailand. Hardy–Weinberg disequilibrium of rs57095329 in the cerebral malaria group showed a heterozygous excess which might be due to natural selection. Conclusion: Our data supported that the candidate microRNA SNPs have no major role to develop cerebral malaria.|
|Appears in Collections:||Scopus 2019|
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