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150 risk variants for diverticular disease of intestine prioritize cell types and enable polygenic prediction of disease susceptibility

We conducted a genome-wide association study (GWAS) analysis of diverticular disease (DivD) of intestine within 724,372 individuals and identified 150 independent genome-wide significant DNA variants. Integration of the GWAS results with human gut single-cell RNA sequencing data implicated gut myocy...

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Autores principales: Wu, Yeda, Goleva, Slavina B., Breidenbach, Lindsay B., Kim, Minsoo, MacGregor, Stuart, Gandal, Michael J., Davis, Lea K., Wray, Naomi R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10363821/
https://www.ncbi.nlm.nih.gov/pubmed/37492107
http://dx.doi.org/10.1016/j.xgen.2023.100326
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author Wu, Yeda
Goleva, Slavina B.
Breidenbach, Lindsay B.
Kim, Minsoo
MacGregor, Stuart
Gandal, Michael J.
Davis, Lea K.
Wray, Naomi R.
author_facet Wu, Yeda
Goleva, Slavina B.
Breidenbach, Lindsay B.
Kim, Minsoo
MacGregor, Stuart
Gandal, Michael J.
Davis, Lea K.
Wray, Naomi R.
author_sort Wu, Yeda
collection PubMed
description We conducted a genome-wide association study (GWAS) analysis of diverticular disease (DivD) of intestine within 724,372 individuals and identified 150 independent genome-wide significant DNA variants. Integration of the GWAS results with human gut single-cell RNA sequencing data implicated gut myocyte, mesothelial and stromal cells, and enteric neurons and glia in DivD development. Ninety-five genes were prioritized based on multiple lines of evidence, including SLC9A3, a drug target gene of tenapanor used for the treatment of the constipation subtype of irritable bowel syndrome. A DivD polygenic score (PGS) enables effective risk prediction (area under the curve [AUC], 0.688; 95% confidence interval [CI], 0.645–0.732) and the top 20% PGS was associated with ∼3.6-fold increased DivD risk relative to the remaining population. Our statistical and bioinformatic analyses suggest that the mechanism of DivD is through colon structure, gut motility, gastrointestinal mucus, and ionic homeostasis. Our analyses reinforce the link between gastrointestinal disorders and the enteric nervous system through genetics.
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spelling pubmed-103638212023-07-25 150 risk variants for diverticular disease of intestine prioritize cell types and enable polygenic prediction of disease susceptibility Wu, Yeda Goleva, Slavina B. Breidenbach, Lindsay B. Kim, Minsoo MacGregor, Stuart Gandal, Michael J. Davis, Lea K. Wray, Naomi R. Cell Genom Article We conducted a genome-wide association study (GWAS) analysis of diverticular disease (DivD) of intestine within 724,372 individuals and identified 150 independent genome-wide significant DNA variants. Integration of the GWAS results with human gut single-cell RNA sequencing data implicated gut myocyte, mesothelial and stromal cells, and enteric neurons and glia in DivD development. Ninety-five genes were prioritized based on multiple lines of evidence, including SLC9A3, a drug target gene of tenapanor used for the treatment of the constipation subtype of irritable bowel syndrome. A DivD polygenic score (PGS) enables effective risk prediction (area under the curve [AUC], 0.688; 95% confidence interval [CI], 0.645–0.732) and the top 20% PGS was associated with ∼3.6-fold increased DivD risk relative to the remaining population. Our statistical and bioinformatic analyses suggest that the mechanism of DivD is through colon structure, gut motility, gastrointestinal mucus, and ionic homeostasis. Our analyses reinforce the link between gastrointestinal disorders and the enteric nervous system through genetics. Elsevier 2023-06-05 /pmc/articles/PMC10363821/ /pubmed/37492107 http://dx.doi.org/10.1016/j.xgen.2023.100326 Text en © 2023 The Authors https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Article
Wu, Yeda
Goleva, Slavina B.
Breidenbach, Lindsay B.
Kim, Minsoo
MacGregor, Stuart
Gandal, Michael J.
Davis, Lea K.
Wray, Naomi R.
150 risk variants for diverticular disease of intestine prioritize cell types and enable polygenic prediction of disease susceptibility
title 150 risk variants for diverticular disease of intestine prioritize cell types and enable polygenic prediction of disease susceptibility
title_full 150 risk variants for diverticular disease of intestine prioritize cell types and enable polygenic prediction of disease susceptibility
title_fullStr 150 risk variants for diverticular disease of intestine prioritize cell types and enable polygenic prediction of disease susceptibility
title_full_unstemmed 150 risk variants for diverticular disease of intestine prioritize cell types and enable polygenic prediction of disease susceptibility
title_short 150 risk variants for diverticular disease of intestine prioritize cell types and enable polygenic prediction of disease susceptibility
title_sort 150 risk variants for diverticular disease of intestine prioritize cell types and enable polygenic prediction of disease susceptibility
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10363821/
https://www.ncbi.nlm.nih.gov/pubmed/37492107
http://dx.doi.org/10.1016/j.xgen.2023.100326
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