Journal Article

Linkage and association of tumor necrosis factor receptor 2 locus with hypertension, hypercholesterolemia and plasma shed receptor

Cheryl L. Glenn, William Y.S. Wang, Adam V. Benjafield and Brian J. Morris

in Human Molecular Genetics

Volume 9, issue 13, pages 1943-1949
Published in print August 2000 | ISSN: 0964-6906
Published online August 2000 | e-ISSN: 1460-2083 | DOI: http://dx.doi.org/10.1093/hmg/9.13.1943
Linkage and association of tumor necrosis factor receptor 2 locus with hypertension, hypercholesterolemia and plasma shed receptor

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Tumor necrosis factor (TNF) receptor 2 (TNF-R2) has been implicated in insulin resistance and metabolic syndrome disorders, one of which is hypertension (HT). We therefore decided to test markers in and near the TNF-R2 gene (TNFRSF1B) for linkage and association with HT, as well as hypercholesterolemia, and plasma levels of the shed soluble receptor (sTNF-R2). The linkage study, which involved 200 HT Anglo-Celtic Caucasian sibpairs, indicated a sharp, significant linkage peak centered at TNFRSF1B (multipoint maximum LOD score = 2.6 and 3.1 by weighted and unweighted MAPMAKER/SIBS, respectively; two-point LOD scores = 2.9 and 3.9 by weighted and unweighted SPLINK, respectively; P = 10–4 by identical-by-state χ2). The case–control study in 134 unrelated HTs who were the offspring of two HT parents and 197 normotensives (NTs) whose parents were both NTs, indicated possible association of TNFRSF1B with HT by haplotype analysis (P = 0.008). Plasma sTNF-R2 was elevated in HTs (P < 0.0001) and showed a correlation with systolic and diastolic blood pressure (BP) (P < 0.0002). A genotypic effect of TNFRSF1B on plasma sTNF-R2, as well as total, low and high density lipoprotein cholesterol, and diastolic BP was observed. These observations are consistent with a scheme leading to raised BP and hypercholesterolemia. In conclusion, TNFRSF1B may be a candidate gene for HT and other metabolic syndrome abnormalities.

Journal Article.  5002 words.  Illustrated.

Subjects: Genetics and Genomics

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