Woraphat Ratta-Apha

Publications (2)11.53 Total impact

• Article: A missense mutation in the ITGA8 gene, a cell adhesion molecule gene, is associated with schizophrenia in Japanese female patients.

  Irwan Supriyanto, Yuichiro Watanabe, Kentaro Mouri, Kyoichi Shiroiwa, Woraphat Ratta-Apha, Masakuni Yoshida, Genki Tamiya, Toru Sasada, Noriomi Eguchi, Kenji Okazaki, Osamu Shirakawa, Toshiyuki Someya, Akitoyo Hishimoto
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  ABSTRACT: BACKGROUND: Cell adhesion molecules (CAMs) play pivotal role in the development of the central nervous system (CNS) and have also been reported to play role in the pathophysiology of schizophrenia. Missense mutations in the CAMs genes might alter the binding of their ligands, increasing the vulnerability to develop schizophrenia. METHODS: We selected 15 missense mutations in the CAMs genes of the CNS reported in the Kyoto Encyclopedia of Genes and Genomes (KEGG) and examined the association between these mutations and schizophrenia in 278 patients and 284 control subjects (first batch). We also genotyped the positive single nucleotide polymorphisms (SNPs) in 567 patients and 710 control subjects (second batch) and in 635 patients and 639 control subjects (replication samples). RESULTS: Genotypic and allelic distributions of rs2298033 in the ITGA8 gene between the schizophrenia and control groups were significantly different in the first batch (p=0.005 and 0.007, respectively). Gender-based analysis revealed that the allelic and genotypic distributions of rs2298033 in the ITGA8 were significantly different between the schizophrenia and control groups among females in both batches (p=0.010, 0.011 and 0.0086, 0.010, respectively) but not among males. Combine analysis of rs2298033 with the replication samples revealed a more significant differences (p=0.0032; 0.0035 in the overall subjects and p=0.0024; 0.0025 in the female subjects, respectively). The significant differences for rs2802808 of the NFASC gene were only observed in the female subgroup of the first batch. CONCLUSION: These results suggest that the ITGA8 gene might have gender-specific roles in the development of schizophrenia. Further replication and functional studies are required to confirm these findings.
  Progress in Neuro-Psychopharmacology and Biological Psychiatry 11/2012; · 3.25 Impact Factor
• Article: Haplotypes in the expression quantitative trait locus of interleukin-1β gene are associated with schizophrenia.

  Masakuni Yoshida, Kyoichi Shiroiwa, Kentaro Mouri, Hiroki Ishiguro, Irwan Supriyanto, Woraphat Ratta-Apha, Noriomi Eguchi, Satoshi Okazaki, Toru Sasada, Masaaki Fukutake, Takeshi Hashimoto, Toshiya Inada, Tadao Arinami, Osamu Shirakawa, Akitoyo Hishimoto
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  ABSTRACT: Recent genome-wide association study (GWAS) and gene expression analyses have revealed that single nucleotide polymorphisms (SNPs) associated with complex diseases such as schizophrenia are significantly more likely to be associated with expression quantitative trait loci (eQTL). The interleukin-1β (IL1B) gene has been strongly implicated in the susceptibility to schizophrenia. In order to test this association, we selected five tag SNPs in the eQTL of the IL1B gene and conducted a case-control study using two independent samples. The first sample comprised 528 schizophrenic patients and 709 controls and the second sample comprised 576 schizophrenic patients and 768 controls. We identified two SNPs and several haplotypes as being significantly associated with schizophrenia. Previous reports indicated that one major haplotype that was protective against schizophrenia reduced IL1B transcription, while two risk haplotypes for schizophrenia enhanced IL1B transcription. Therefore, we measured IL1B mRNA expression in PAXgene-stabilized whole blood from 40 schizophrenic patients and 40 controls to explore the possibility of using five tag SNPs as schizophrenic trait markers. A multiple regression analysis taking confounding factors into account revealed that the T allele of rs4848306 SNP, which is a protective allele for schizophrenia, predicted reduced change in IL1B mRNA expression, regardless of phenotype. Our results appear to support the previous hypothesis that IL1B contributes to the genetic risk of schizophrenia and warrant further research on the association of eQTL SNPs with schizophrenia.
  Biological Psychiatry 07/2012; 140(1-3):185-91. · 8.28 Impact Factor