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L-006 GENOME-WIDE SCAN FOR YOUNG-ONSET HYPERTENSION IN HAN CHINESE IN TAIWAN

Background Hypertension is an important public health issue in Taiwan. Efforts to map hypertension genes have been proven difficult without large sample size and phenotype with strong genetic component. The purpose of our study is to carry out a genome-wide linkage study with young-onset hypertension as the phenotype and followed by single nucleotide polymorphism (SNP) fine mapping of candidate genes in the linked chromosomal region to identify novel genes for hypertension. Methods We have recruited 1447 individuals, including 675 affected patients from 464 families. The maker set of deCODE genetics that defines a ∼10 centi Morgan (cM) resolution in human index map was typed for study subjects. Evidence of linkage was assessed with a non-parametric linkage method using GENEHUNTER. Two point linkage analyses were calculated, using the SIBPAL program. We then used tag SNPs selected from public HapMap database for all genes in these candidate regions to pin down the hypertension susceptibility gene. Genotyping for a total of 27 SNPs was obtained using mass spectrometer-based detection implemented on a Sequenom Mass ARRAY system. Transmission disequilibrium test (TDT) analysis implemented in GENEHUNTER was performed for fine mapping. Result Indication of linkage signals were demonstrated consistently by two methods for regions on chromosome 1, 2, 3, 4, 6, 7, 8, 19, and 22. Among them, a region on chromosome 2 with a NPL score over 2 overlaps with findings of several other studies. There are several other novel positions identified by our study, including three with NPL score over or close to 1.5. In the fine mapping stage, we found the haplo type constructed by 3 markers flanking the region for POLR1B, CHCHD5, SLC20A and FLJ40629 on chromosome 2 and another haplotype constructed by 2 SNPs on SI gene on chromosome 3 were associated with hypertension (p = 0.000037 and P = 0.019 respectively). Gene expressions of those genes were significantly (P < .01) higher in lymphocyte cells from hypertensive patients than from controls. Conclusion These results advance understanding of the genetic basis of hypertension.