Resequencing Study Confirms That Host Defense and Cell Senescence Gene Variants Contribute to the Risk of Idiopathic Pulmonary Fibrosis
Several common and rare genetic variants have been associated with idiopathic pulmonary fibrosis, a progressive fibrotic condition that is localized to the lung. To develop an integrated understanding of the rare and common variants located in multiple loci that have been reported to contribute to t...
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| Published in | American journal of respiratory and critical care medicine Vol. 200; no. 2; pp. 199 - 208 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Thoracic Society
15.07.2019
|
| Subjects | |
| Online Access | Get full text |
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| Abstract | Several common and rare genetic variants have been associated with idiopathic pulmonary fibrosis, a progressive fibrotic condition that is localized to the lung.
To develop an integrated understanding of the rare and common variants located in multiple loci that have been reported to contribute to the risk of disease.
We performed deep targeted resequencing (3.69 Mb of DNA) in cases (
= 3,624) and control subjects (
= 4,442) across genes and regions previously associated with disease. We tested for associations between disease and
) individual common variants via logistic regression and
) groups of rare variants via sequence kernel association tests.
Statistically significant common variant association signals occurred in all 10 of the regions chosen based on genome-wide association studies. The strongest risk variant is the
promoter variant rs35705950, with an odds ratio of 5.45 (95% confidence interval, 4.91-6.06) for one copy of the risk allele and 18.68 (95% confidence interval, 13.34-26.17) for two copies of the risk allele (
= 9.60 × 10
). In addition to identifying for the first time that rare variation in
is associated with disease, we confirmed the role of rare variation in the
and
gene regions in the risk of IPF, and found that the
and
regions have independent common and rare variant signals.
A limited number of common and rare variants contribute to the risk of idiopathic pulmonary fibrosis in each of the resequencing regions, and these genetic variants focus on biological mechanisms of host defense and cell senescence. |
|---|---|
| AbstractList | Several common and rare genetic variants have been associated with idiopathic pulmonary fibrosis, a progressive fibrotic condition that is localized to the lung.
To develop an integrated understanding of the rare and common variants located in multiple loci that have been reported to contribute to the risk of disease.
We performed deep targeted resequencing (3.69 Mb of DNA) in cases (
= 3,624) and control subjects (
= 4,442) across genes and regions previously associated with disease. We tested for associations between disease and
) individual common variants via logistic regression and
) groups of rare variants via sequence kernel association tests.
Statistically significant common variant association signals occurred in all 10 of the regions chosen based on genome-wide association studies. The strongest risk variant is the
promoter variant rs35705950, with an odds ratio of 5.45 (95% confidence interval, 4.91-6.06) for one copy of the risk allele and 18.68 (95% confidence interval, 13.34-26.17) for two copies of the risk allele (
= 9.60 × 10
). In addition to identifying for the first time that rare variation in
is associated with disease, we confirmed the role of rare variation in the
and
gene regions in the risk of IPF, and found that the
and
regions have independent common and rare variant signals.
A limited number of common and rare variants contribute to the risk of idiopathic pulmonary fibrosis in each of the resequencing regions, and these genetic variants focus on biological mechanisms of host defense and cell senescence. Rationale: Several common and rare genetic variants have been associated with idiopathic pulmonary fibrosis, a progressive fibrotic condition that is localized to the lung. Objectives: To develop an integrated understanding of the rare and common variants located in multiple loci that have been reported to contribute to the risk of disease. Methods: We performed deep targeted resequencing (3.69 Mb of DNA) in cases (n = 3,624) and control subjects (n = 4,442) across genes and regions previously associated with disease. We tested for associations between disease and 1) individual common variants via logistic regression and 2) groups of rare variants via sequence kernel association tests. Measurements and Main Results: Statistically significant common variant association signals occurred in all 10 of the regions chosen based on genome-wide association studies. The strongest risk variant is the MUC5B promoter variant rs35705950, with an odds ratio of 5.45 (95% confidence interval, 4.91–6.06) for one copy of the risk allele and 18.68 (95% confidence interval, 13.34–26.17) for two copies of the risk allele (P = 9.60 × 10−295). In addition to identifying for the first time that rare variation in FAM13A is associated with disease, we confirmed the role of rare variation in the TERT and RTEL1 gene regions in the risk of IPF, and found that the FAM13A and TERT regions have independent common and rare variant signals. Conclusions: A limited number of common and rare variants contribute to the risk of idiopathic pulmonary fibrosis in each of the resequencing regions, and these genetic variants focus on biological mechanisms of host defense and cell senescence. Rationale: Several common and rare genetic variants have been associated with idiopathic pulmonary fibrosis, a progressive fibrotic condition that is localized to the lung. Objectives: To develop an integrated understanding of the rare and common variants located in multiple loci that have been reported to contribute to the risk of disease. Methods: We performed deep targeted resequencing (3.69 Mb of DNA) in cases (n = 3,624) and control subjects (n = 4,442) across genes and regions previously associated with disease. We tested for associations between disease and 1) individual common variants via logistic regression and 2) groups of rare variants via sequence kernel association tests. Measurements and Main Results: Statistically significant common variant association signals occurred in all 10 of the regions chosen based on genome-wide association studies. The strongest risk variant is the MUC5B promoter variant rs35705950, with an odds ratio of 5.45 (95% confidence interval, 4.91-6.06) for one copy of the risk allele and 18.68 (95% confidence interval, 13.34-26.17) for two copies of the risk allele (P = 9.60 × 10-295). In addition to identifying for the first time that rare variation in FAM13A is associated with disease, we confirmed the role of rare variation in the TERT and RTEL1 gene regions in the risk of IPF, and found that the FAM13A and TERT regions have independent common and rare variant signals. Conclusions: A limited number of common and rare variants contribute to the risk of idiopathic pulmonary fibrosis in each of the resequencing regions, and these genetic variants focus on biological mechanisms of host defense and cell senescence.Rationale: Several common and rare genetic variants have been associated with idiopathic pulmonary fibrosis, a progressive fibrotic condition that is localized to the lung. Objectives: To develop an integrated understanding of the rare and common variants located in multiple loci that have been reported to contribute to the risk of disease. Methods: We performed deep targeted resequencing (3.69 Mb of DNA) in cases (n = 3,624) and control subjects (n = 4,442) across genes and regions previously associated with disease. We tested for associations between disease and 1) individual common variants via logistic regression and 2) groups of rare variants via sequence kernel association tests. Measurements and Main Results: Statistically significant common variant association signals occurred in all 10 of the regions chosen based on genome-wide association studies. The strongest risk variant is the MUC5B promoter variant rs35705950, with an odds ratio of 5.45 (95% confidence interval, 4.91-6.06) for one copy of the risk allele and 18.68 (95% confidence interval, 13.34-26.17) for two copies of the risk allele (P = 9.60 × 10-295). In addition to identifying for the first time that rare variation in FAM13A is associated with disease, we confirmed the role of rare variation in the TERT and RTEL1 gene regions in the risk of IPF, and found that the FAM13A and TERT regions have independent common and rare variant signals. Conclusions: A limited number of common and rare variants contribute to the risk of idiopathic pulmonary fibrosis in each of the resequencing regions, and these genetic variants focus on biological mechanisms of host defense and cell senescence. Rationale: Several common and rare genetic variants have been associated with idiopathic pulmonary fibrosis, a progressive fibrotic condition that is localized to the lung. Objectives: To develop an integrated understanding of the rare and common variants located in multiple loci that have been reported to contribute to the risk of disease. Methods: We performed deep targeted resequencing (3.69 Mb of DNA) in cases ( n = 3,624) and control subjects ( n = 4,442) across genes and regions previously associated with disease. We tested for associations between disease and 1 ) individual common variants via logistic regression and 2 ) groups of rare variants via sequence kernel association tests. Measurements and Main Results: Statistically significant common variant association signals occurred in all 10 of the regions chosen based on genome-wide association studies. The strongest risk variant is the MUC5B promoter variant rs35705950, with an odds ratio of 5.45 (95% confidence interval, 4.91–6.06) for one copy of the risk allele and 18.68 (95% confidence interval, 13.34–26.17) for two copies of the risk allele ( P = 9.60 × 10 −295 ). In addition to identifying for the first time that rare variation in FAM13A is associated with disease, we confirmed the role of rare variation in the TERT and RTEL1 gene regions in the risk of IPF, and found that the FAM13A and TERT regions have independent common and rare variant signals. Conclusions: A limited number of common and rare variants contribute to the risk of idiopathic pulmonary fibrosis in each of the resequencing regions, and these genetic variants focus on biological mechanisms of host defense and cell senescence. |
| Author | Mogulkoc, Nesrin Powers, Julie Glaspole, Ian Ma, Shwu-Fan Vašáková, Martina Moore, Camille Henry, Michael T. Machahua, Carlos Inoue, Yoshikazu Blumhagen, Rachel Z. Gudmundsson, Gunnar Furusawa, Haruhiko Kim, Dong Soon Kreider, Maryl E. Walker, Tarik Cho, Michael H. Montesi, Sydney B. Brown, Kevin K. Fernandez, Isis Enlil Fiddler, Christine Steele, Mark P. Kim, Hocheol Akagawa, Shinobu Lederer, David J. Song, Jin Woo Wilcox, Pearce G. Cogan, Joy D. Baltic, Svetlana Prele, Cecilia Russell, Pamela Porteous, Mary K. Pacheco, Karin A. Selman, Moises Podolanczuk, Anna J. Bishop, Makenna Strek, Mary E. Guthridge, Joel M. Mathai, Susan K. Silverman, Edwin K. Zhang, Yingze Okamoto, Tsukasa Worboys, Ana Montes Tomassetti, Sara Sundy, John S. Molyneaux, Philip L. Isaksson, Helgi J. Laurent, Geoffrey Wolters, Paul J. Saunders, Peter Yang, Ivana V. Maier, Lisa A. Eickelberg, Oliver Markin, Cheryl R. Doran, Peter James, Judith A. O’Riordan, Thomas Li, Feng Sterclova, Martina Pardo, Annie Poletti, Venerino Braybrooke, Rebecca Sembrat, John Gibson, Kevin F. Colla |
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Yingze organization: Simmons Center for Interstitial Lung Disease, University of Pittsburgh, Pittsburgh, Pennsylvania – sequence: 43 givenname: Kevin F. surname: Gibson fullname: Gibson, Kevin F. organization: Simmons Center for Interstitial Lung Disease, University of Pittsburgh, Pittsburgh, Pennsylvania – sequence: 44 givenname: Daniel J. surname: Kass fullname: Kass, Daniel J. organization: Simmons Center for Interstitial Lung Disease, University of Pittsburgh, Pittsburgh, Pennsylvania – sequence: 45 givenname: Mauricio surname: Rojas fullname: Rojas, Mauricio organization: Simmons Center for Interstitial Lung Disease, University of Pittsburgh, Pittsburgh, Pennsylvania – sequence: 46 givenname: John surname: Sembrat fullname: Sembrat, John organization: Simmons Center for Interstitial Lung Disease, University of Pittsburgh, Pittsburgh, Pennsylvania – sequence: 47 givenname: Paul J. surname: Wolters fullname: Wolters, Paul J. organization: Department of Medicine, University of California, San Francisco, San Francisco, California – sequence: 48 givenname: Harold R. surname: Collard fullname: Collard, Harold R. organization: Department of Medicine, University of California, San Francisco, San Francisco, California – sequence: 49 givenname: John S. surname: Sundy fullname: Sundy, John S. organization: Gilead Sciences, Foster City, California – sequence: 50 givenname: Thomas surname: O’Riordan fullname: O’Riordan, Thomas organization: Gilead Sciences, Foster City, California – sequence: 51 givenname: Mary E. surname: Strek fullname: Strek, Mary E. organization: Department of Medicine, University of Chicago, Chicago, Illinois – sequence: 52 givenname: Imre surname: Noth fullname: Noth, Imre organization: Department of Medicine, University of Virginia, Charlottesville, Virginia – sequence: 53 givenname: Shwu-Fan surname: Ma fullname: Ma, Shwu-Fan organization: Department of Medicine, University of Virginia, Charlottesville, Virginia – sequence: 54 givenname: Mary K. surname: Porteous fullname: Porteous, Mary K. organization: Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania – sequence: 55 givenname: Maryl E. surname: Kreider fullname: Kreider, Maryl E. organization: Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania – sequence: 56 givenname: Namrata B. surname: Patel fullname: Patel, Namrata B. organization: Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania – sequence: 57 givenname: Yoshikazu orcidid: 0000-0003-3994-874X surname: Inoue fullname: Inoue, Yoshikazu organization: National Hospital Organization Kinki-Chuo Chest Medical Center, Osaka, Japan – sequence: 58 givenname: Masaki surname: Hirose fullname: Hirose, Masaki organization: National Hospital Organization Kinki-Chuo Chest Medical Center, Osaka, Japan – sequence: 59 givenname: Toru surname: Arai fullname: Arai, Toru organization: National Hospital Organization 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Sydney, Australia – sequence: 66 givenname: Ian surname: Glaspole fullname: Glaspole, Ian organization: Alfred Hospital and Monash University, Melbourne, Australia – sequence: 67 givenname: Sara surname: Tomassetti fullname: Tomassetti, Sara organization: Pulmonary Medicine, GB Morgagni Hospital, Forlì, Italy – sequence: 68 givenname: Claudia surname: Ravaglia fullname: Ravaglia, Claudia organization: Department of Diseases of the Thorax, Ospedale GB Morgagni, Forlì, Italy – sequence: 69 givenname: Venerino surname: Poletti fullname: Poletti, Venerino organization: Department of Diseases of the Thorax, Ospedale GB Morgagni, Forlì, Italy – sequence: 70 givenname: Bruno surname: Crestani fullname: Crestani, Bruno organization: Université Paris Diderot and Hôpital Bichat, Paris, France – sequence: 71 givenname: Raphael surname: Borie fullname: Borie, Raphael organization: Université Paris Diderot and Hôpital Bichat, Paris, France – sequence: 72 givenname: Caroline surname: Kannengiesser 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surname: Ryerson fullname: Ryerson, Christopher J. organization: University of British Columbia, Vancouver, Canada – sequence: 94 givenname: Pearce G. surname: Wilcox fullname: Wilcox, Pearce G. organization: University of British Columbia, Vancouver, Canada – sequence: 95 givenname: Tsukasa surname: Okamoto fullname: Okamoto, Tsukasa organization: Department of Medicine, and, Tokyo Medical and Dental University, Tokyo, Japan – sequence: 96 givenname: Haruhiko surname: Furusawa fullname: Furusawa, Haruhiko organization: Department of Medicine, and, Tokyo Medical and Dental University, Tokyo, Japan – sequence: 97 givenname: Yasunari surname: Miyazaki fullname: Miyazaki, Yasunari organization: Tokyo Medical and Dental University, Tokyo, Japan – sequence: 98 givenname: Geoffrey surname: Laurent fullname: Laurent, Geoffrey organization: Institute for Respiratory Health and, Centre for Cell Therapy and Regenerative Medicine, School of Biomedical Sciences, The University of Western Australia, Perth, Australia – sequence: 99 givenname: Svetlana surname: Baltic fullname: Baltic, Svetlana organization: Institute for Respiratory Health and – sequence: 100 givenname: Cecilia surname: Prele fullname: Prele, Cecilia organization: Institute for Respiratory Health and, Centre for Cell Therapy and Regenerative Medicine, School of Biomedical Sciences, The University of Western Australia, Perth, Australia |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31034279$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1111/resp.12466 10.1164/rccm.201509-1863OC 10.1038/ng.2609 10.1164/rccm.201509-1872LE 10.1016/j.ajhg.2012.06.007 10.1056/NEJM200102223440805 10.1016/S2213-2600(13)70045-6 10.1056/NEJMoa066157 10.1038/nrdp.2017.74 10.1164/rccm.201807-1255ST 10.1186/s12863-016-0377-2 10.1038/ng.3752 10.1056/NEJMoa1013660 10.1016/S2213-2600(17)30387-9 10.1038/nature24277 10.1073/pnas.0901259106 10.1165/rcmb.2017-0046OC 10.4161/fly.19695 10.1038/ng.3278 10.1073/pnas.0701009104 10.1371/journal.pone.0104919 10.1016/j.ajhg.2008.11.010 10.1093/nar/gkx1098 10.1126/science.1200120 10.1126/science.1223012 10.1152/physrev.00004.2016 10.1016/S2213-2600(18)30135-8 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Deceased. These authors contributed equally as senior authors. These authors contributed equally as first authors. T.M.M., H.R.C., and O.E. are Associate Editors of AJRCCM. Their participation complies with American Thoracic Society requirements for recusal from review and decisions for authored works. |
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| References | bib14 bib12 bib13 bib10 bib11 bib29 bib28 bib25 bib26 bib23 bib24 bib21 bib22 bib20 bib9 bib7 bib8 bib5 bib18 bib6 bib19 bib3 bib16 bib4 bib17 bib1 bib2 31113211 - Am J Respir Crit Care Med. 2019 Jul 15;200(2):125-127. doi: 10.1164/rccm.201905-0925ED. |
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| Snippet | Several common and rare genetic variants have been associated with idiopathic pulmonary fibrosis, a progressive fibrotic condition that is localized to the... Rationale: Several common and rare genetic variants have been associated with idiopathic pulmonary fibrosis, a progressive fibrotic condition that is localized... Rationale: Several common and rare genetic variants have been associated with idiopathic pulmonary fibrosis, a progressive fibrotic condition that is localized... |
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| SubjectTerms | ATP-Binding Cassette Transporters - genetics Case-Control Studies Cellular Senescence - genetics DNA Helicases - genetics Exoribonucleases - genetics Family medical history Female Gene loci Genealogy Genetic Predisposition to Disease Genetic Variation Genome-Wide Association Study Genomes Genomics GTPase-Activating Proteins - genetics High-Throughput Nucleotide Sequencing Hospitals Host-Pathogen Interactions - genetics Humans Idiopathic Pulmonary Fibrosis - genetics Logistic Models Lung diseases Male Medicine Mucin-5B - genetics Mutation Original Promoter Regions, Genetic - genetics Pulmonary fibrosis Pulmonary Surfactant-Associated Protein A - genetics Pulmonary Surfactant-Associated Protein C - genetics RNA - genetics Senescence Sequence Analysis, DNA Telomerase - genetics Telomere-Binding Proteins - genetics University colleges |
| Title | Resequencing Study Confirms That Host Defense and Cell Senescence Gene Variants Contribute to the Risk of Idiopathic Pulmonary Fibrosis |
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