从 GWAS 基因座到血压基因、变异-猫眼课题宝

从 GWAS 基因座到血压基因、变异

批准号：

10659683

负责人：

ARAVINDA CHAKRAVARTI

金额：

$125.56万

依托单位：

NEW YORK UNIVERSITY SCHOOL OF MEDICINE

依托单位国家：

美国

项目类别：

财政年份：

2007

资助国家：

美国

项目状态：

未结题

起止时间：

2007-09-01 至 2027-03-31

来源：

https://reporter.nih.gov/project-details/10659683

关键词：

Adrenal Glands Affect Aorta Architecture Biological Assay Blood Pressure Blood Vessels Chromatin Clinical Collaborations Common Core Data Defect Dissection Endothelial Cells Endothelium Enhancers Gene Expression Gene Expression Profile Generations Genes Genetic Polymorphism Genetic Research Genome Genomics Genotype Genotype-Tissue Expression Project Goals Heart Heritability Human Hypertension Individual International Kidney Laboratories Machine Learning Maps Methods National Heart, Lung, and Blood Institute Nitric Oxide Organ Participant Pathogenicity Physiological Publishing Pulse Pressure Regulator Genes Regulatory Element Research Risk Risk Factors Seminal Small Interfering RNA Testing Tissues Trans-Omics for Precision Medicine Umbilical vein United States National Institutes of Health Validation Variant Vascular Smooth Muscle blood pressure control blood pressure regulation cell type cohort endothelial dysfunction epidemiology study epigenome exome functional genomics gene function gene regulatory network genome wide association study genome-wide human tissue in vitro Assay inter-individual variation knock-down machine learning method novel phenotypic data pleiotropism programs trait transcription factor transcriptome sequencing vascular contributions

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Defects in systolic (S) and diastolic (D) blood pressure (BP) regulation underlie clinical hypertension and its subsequent target organ damage when unrecognized and untreated. Over the past 15 years, we have been major contributors to the genomic analyses of BP enabling dissection of inter-individual SBP and DBP variation, through this FEHGAS research program in collaboration with national/international consortia. While the major approach has been to further expand GWAS, in this renewal (FEHGAS4), we introduce an alternative novel program of using genome-cum-epigenome screens to quantify the contributions of each tissue and cell type to causal BP variation through their transcription factors (TFs), cognate cis regulatory elements (CREs) and target genes, organized into gene regulatory networks (GRNs). Our preliminary studies suggest significant contributions by arterial-, heart-, adrenal- and kidney- specific regulatory variants in decreasing order. In this proposal we ask: (1) Which tissues and cell types contribute to SBP and DBP variation between humans? (2) Which genes in a tissue/cell type contribute to human SBP and DBP control? (3) What is the functional architecture of inter-individual SBP and DBP variation? (4) What is the differential tissue contribution to risk. 1

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