Quantitative trait locus mapping of human blood pressure to a genetic region at or near the lipoprotein lipase gene locus on chromosome 8p22.

Wu, Der-Min; Bu, Xingyao; Warden, Craig H; Shen, David; Jeng, Chii; Sheu, Wayne H‐H; Fuh, Martin Mao-Tsu; Katsuya, Tomohiro; Dzau, Victor J.; Reaven, Gerald M.; Lusis, Aldons J.; Rotter, Jerome I.; Chen, Y.-D. I.

doi:10.1172/jci118648

Cited by 110 publications

(70 citation statements)

References 46 publications

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“…They also failed to find any suggestive linkage between a-adducin gene and EH or the gene-gene interactions. In our study, D4S412 and D4S3038, 15 In the present study, however, the results cannot be replicated in an extended sample size of 108 Shanghai EH families. We also failed to find a linkage between the other four gene loci (OB, OBR, ADRB3 and LPL) and EH, although some significant linkage was reported in other populations (Table 4).…”

Section: Discussioncontrasting

confidence: 80%

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Linkage analysis of five candidate genes and essential hypertension in 106 Chinese nuclear families

Wang

Huang

et al. 2003

J Hum Hypertens

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Five candidate genes including the lipoprotein lipase, leptin, leptin receptor, a-adducin and b3 adrenergic receptor were selected to examine their possible contribution to essential hypertension (EH) in a Chinese population. On each side of the candidate gene loci, one to two highly polymorphic microsatellite markers were genotyped in 474 subjects recruited from 106 hypertension nuclear families in Shanghai. Both parametric and nonparametric linkage analyses were carried out using GENEHUNTER (version 2.0) after genotyping. Extended transmission disequilibrium testing (ETDT) was also conducted to detect preferential transmission of alleles to affected offspring. We failed to find the linkage between all these loci and EH by either parametric or nonparametric analysis, nor did we detect any significant transmission disequilibrium by ETDT. Our findings provide no support for a significant contribution of these five genes to the pathogenesis of EH among Shanghai people.

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Section: Discussioncontrasting

confidence: 80%

“…Although the products of these five EH candidate genes act in the field of sodium balance or neuro-endocrine modulation, their actual roles in the pathogenesis of EH remain unknown. [14][15][16][17][18][19] Especially for the two genes OBR and ARBR3, no linkage study has been reported yet.…”

Section: Discussionmentioning

confidence: 99%

Linkage analysis of five candidate genes and essential hypertension in 106 Chinese nuclear families

Wang

Huang

et al. 2003

J Hum Hypertens

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“…This may reflect difficulties in the replication of supportive findings under complex circumstances modulating hypertension, such as the heterogeneous nature of genetic susceptibility and gene-environment interactions. 6 The affected sib-pair method has revealed that angiotensinogen, lipoprotein lipase and ␣-adducin gene polymorphisms are genetic risk factors for human essential hypertension, [7][8][9] but no specific gene clearly governing susceptibility for hypertension has yet been identified. The low-density lipoprotein (LDL) receptor is one candidate that plays an integral role in plasma lipoprotein metabolism.…”

Section: Journal Of Human Hypertension (2001) 15 125-130mentioning

confidence: 99%

A common mutation of low-density lipoprotein receptor gene is associated with essential hypertension among Japanese

Katsuya

Higaki

et al. 2001

J Hum Hypertens

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Candidate genes offer one approach to the identification of the genetic susceptibility to hypertension. A common gene variant of the low-density lipoprotein (LDL) receptor gene (LDLR) that affects plasma LDL metabolism within the normolipidaemic range, may be such a candidate gene. A common mutation of LDLR, C1773T, was associated with lipid metabolism such that the T1773 allele increased plasma LDL levels in a Caucasian population. The present study examined whether C1773T/LDLR was associated with essential hypertension in a Japanese population. Subjects with essential hypertension (EHT, n = 300) with a family history of hypertension, and controls (NT, n = 310, sex-and agematched with EHT) were recruited from among outpatients at Osaka University Hospital. A C1773T substitution at codon 570 in LDLR was determined using PCR-

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“…Marker LPL1GTR2, located in the 5Ј region of the LPL gene, is described in detail in Odelberg and White. 23 D8S282 is 3 cM from the LPL gene and is described in Wu et al 24 Polymerase chain reactions for the markers were carried out by use of standard techniques and under standard conditions optimized for each marker. Exact concentrations and conditions are available on request from the authors.…”

Section: Genotypingmentioning

confidence: 99%

Replication of Linkage of Familial Combined Hyperlipidemia to Chromosome 1q With Additional Heterogeneous Effect of Apolipoprotein A-I/C-III/A-IV Locus

Coon

Myers

Borecki

et al. 2000

ATVB

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Abstract-Familial combined hyperlipidemia (FCHL), the most common familial dyslipidemia, is implicated in up to 20% of cases of premature coronary heart disease. Although underlying mutations for FCHL have yet to be identified, several candidate genes/regions have been identified. A positive linkage to chromosome 1q markers has been reported, with the highest lod score of 5.93 occurring at a location between D1S104 and D1S1677. Using the same diagnostic criteria, the Family Heart Study (FHS) has defined 71 FCHL families, comprising 170 cases, for a total of 137 possible affected sibling pairs. The FCHL criteria require elevation in serum low density lipoprotein cholesterol and triglyceride levels within the family, with at least 2 affected first-degree relatives. Markers D1S104 and D1S1677 were typed, and significant allele sharing was found in FCHL sibships (multipoint lod score with use of the model from the Finnish study was 2.52, and multipoint nonparametric score was 2.48; Pϭ0.007), replicating linkage in this chromosome 1 region. In addition, previously reported linkage of FCHL to apolipoprotein A-I/C-III/A-IV has been investigated in FHS families. FHS results revealed positive but nonsignificant allele sharing among FCHL sibships with apolipoprotein A-I/C-III/ A-IV by use of marker D11S4127 (nonparametric linkage score 1.11, Pϭ0.13). Two-locus analyses of D1S104 and D11S4127 suggested possible heterogeneity rather than epistasis, with a maximum 2-locus lod score of 3.05. A nonparametric 2-locus analysis revealed significant improvement in the 2-locus versus single-locus scores. Key Words: genetic linkage Ⅲ coronary disease Ⅲ hyperlipidemia F amilial combined hyperlipidemia (FCHL) is the most common familial dyslipidemia, with a prevalence of 1% to 2%, 1 and is implicated in up to 20% of cases of premature coronary heart disease (CHD). 2 FCHL criteria require elevation of serum total cholesterol and triglyceride levels within the family, with at least 2 affected first-degree relatives. 3 Studies of the genetics of FCHL have been complicated by uncertain phenotype definition, likely genetic heterogeneity, and unknown mode of inheritance. These difficulties have thus far prevented the identification of underlying mutations for FCHL. Several loci have produced positive results, although often with mixed findings in replication studies.Perhaps the most promising candidate region is on chromosome 1q21-23. Pajukanta et al 4 recently published positive linkage to chromosome 1q markers in 250 individuals (115 affected) from 31 Finnish FCHL families, with the highest lod score of 5.93 occurring between D1S104 and D1S1677.

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Quantitative trait locus mapping of human blood pressure to a genetic region at or near the lipoprotein lipase gene locus on chromosome 8p22.

Cited by 110 publications

References 46 publications

Linkage analysis of five candidate genes and essential hypertension in 106 Chinese nuclear families

Linkage analysis of five candidate genes and essential hypertension in 106 Chinese nuclear families

A common mutation of low-density lipoprotein receptor gene is associated with essential hypertension among Japanese

Replication of Linkage of Familial Combined Hyperlipidemia to Chromosome 1q With Additional Heterogeneous Effect of Apolipoprotein A-I/C-III/A-IV Locus

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