Network study of nasal transcriptome profiles reveals master regulator genes of asthma
Nasal transcriptomics can provide an accessible window into asthma pathobiology. Our goal was to move beyond gene signatures of asthma to identify master regulator genes that causally regulate genes associated with asthma phenotypes. We recruited 156 children with severe persistent asthma and contro...
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| Vydané v: | Journal of allergy and clinical immunology Ročník 147; číslo 3; s. 879 - 893 |
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| Hlavní autori: | , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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United States
Elsevier Inc
01.03.2021
Elsevier Limited |
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| ISSN: | 0091-6749, 1097-6825, 1097-6825 |
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| Abstract | Nasal transcriptomics can provide an accessible window into asthma pathobiology.
Our goal was to move beyond gene signatures of asthma to identify master regulator genes that causally regulate genes associated with asthma phenotypes.
We recruited 156 children with severe persistent asthma and controls for nasal transcriptome profiling and applied network-based and probabilistic causal methods to identify severe asthma genes and their master regulators. We then took the same approach in an independent cohort of 190 adults with mild/moderate asthma and controls to identify mild/moderate asthma genes and their master regulators. Comparative analysis of the master regulator genes followed by validation testing in independent children with severe asthma (n = 21) and mild/moderate asthma (n = 154) was then performed.
Nasal gene signatures for severe persistent asthma and for mild/moderate persistent asthma were identified; both were found to be enriched in coexpression network modules for ciliary function and inflammatory response. By applying probabilistic causal methods to these gene signatures and validation testing in independent cohorts, we identified (1) a master regulator gene common to asthma across severity and ages (FOXJ1); (2) master regulator genes of severe persistent asthma in children (LRRC23, TMEM231, CAPS, PTPRC, and FYB); and (3) master regulator genes of mild/moderate persistent asthma in children and adults (C1orf38 and FMNL1). The identified master regulators were statistically inferred to causally regulate the expression of downstream genes that modulate ciliary function and inflammatory response to influence asthma.
The identified master regulator genes of asthma provide a novel path forward to further uncovering asthma mechanisms and therapy.
[Display omitted] |
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| AbstractList | Nasal transcriptomics can provide an accessible window into asthma pathobiology.
Our goal was to move beyond gene signatures of asthma to identify master regulator genes that causally regulate genes associated with asthma phenotypes.
We recruited 156 children with severe persistent asthma and controls for nasal transcriptome profiling and applied network-based and probabilistic causal methods to identify severe asthma genes and their master regulators. We then took the same approach in an independent cohort of 190 adults with mild/moderate asthma and controls to identify mild/moderate asthma genes and their master regulators. Comparative analysis of the master regulator genes followed by validation testing in independent children with severe asthma (n = 21) and mild/moderate asthma (n = 154) was then performed.
Nasal gene signatures for severe persistent asthma and for mild/moderate persistent asthma were identified; both were found to be enriched in coexpression network modules for ciliary function and inflammatory response. By applying probabilistic causal methods to these gene signatures and validation testing in independent cohorts, we identified (1) a master regulator gene common to asthma across severity and ages (FOXJ1); (2) master regulator genes of severe persistent asthma in children (LRRC23, TMEM231, CAPS, PTPRC, and FYB); and (3) master regulator genes of mild/moderate persistent asthma in children and adults (C1orf38 and FMNL1). The identified master regulators were statistically inferred to causally regulate the expression of downstream genes that modulate ciliary function and inflammatory response to influence asthma.
The identified master regulator genes of asthma provide a novel path forward to further uncovering asthma mechanisms and therapy.
[Display omitted] Network study of nasal transcriptome profiles from multiple human cohorts identified nasal gene signatures for severe persistent asthma, mild/moderate persistent asthma, and master regulator genes of asthma. Nasal transcriptomics can provide an accessible window into asthma pathobiology. Our goal was to move beyond gene signatures of asthma to identify master regulator genes that causally regulate genes associated with asthma phenotypes. We recruited 156 children with severe persistent asthma and controls for nasal transcriptome profiling and applied network-based and probabilistic causal methods to identify severe asthma genes and their master regulators. We then took the same approach in an independent cohort of 190 adults with mild/moderate asthma and controls to identify mild/moderate asthma genes and their master regulators. Comparative analysis of the master regulator genes followed by validation testing in independent children with severe asthma (n = 21) and mild/moderate asthma (n = 154) was then performed. Nasal gene signatures for severe persistent asthma and for mild/moderate persistent asthma were identified; both were found to be enriched in coexpression network modules for ciliary function and inflammatory response. By applying probabilistic causal methods to these gene signatures and validation testing in independent cohorts, we identified (1) a master regulator gene common to asthma across severity and ages (FOXJ1); (2) master regulator genes of severe persistent asthma in children (LRRC23, TMEM231, CAPS, PTPRC, and FYB); and (3) master regulator genes of mild/moderate persistent asthma in children and adults (C1orf38 and FMNL1). The identified master regulators were statistically inferred to causally regulate the expression of downstream genes that modulate ciliary function and inflammatory response to influence asthma. The identified master regulator genes of asthma provide a novel path forward to further uncovering asthma mechanisms and therapy. Nasal transcriptomics can provide an accessible window into asthma pathobiology.BACKGROUNDNasal transcriptomics can provide an accessible window into asthma pathobiology.Our goal was to move beyond gene signatures of asthma to identify master regulator genes that causally regulate genes associated with asthma phenotypes.OBJECTIVEOur goal was to move beyond gene signatures of asthma to identify master regulator genes that causally regulate genes associated with asthma phenotypes.We recruited 156 children with severe persistent asthma and controls for nasal transcriptome profiling and applied network-based and probabilistic causal methods to identify severe asthma genes and their master regulators. We then took the same approach in an independent cohort of 190 adults with mild/moderate asthma and controls to identify mild/moderate asthma genes and their master regulators. Comparative analysis of the master regulator genes followed by validation testing in independent children with severe asthma (n = 21) and mild/moderate asthma (n = 154) was then performed.METHODSWe recruited 156 children with severe persistent asthma and controls for nasal transcriptome profiling and applied network-based and probabilistic causal methods to identify severe asthma genes and their master regulators. We then took the same approach in an independent cohort of 190 adults with mild/moderate asthma and controls to identify mild/moderate asthma genes and their master regulators. Comparative analysis of the master regulator genes followed by validation testing in independent children with severe asthma (n = 21) and mild/moderate asthma (n = 154) was then performed.Nasal gene signatures for severe persistent asthma and for mild/moderate persistent asthma were identified; both were found to be enriched in coexpression network modules for ciliary function and inflammatory response. By applying probabilistic causal methods to these gene signatures and validation testing in independent cohorts, we identified (1) a master regulator gene common to asthma across severity and ages (FOXJ1); (2) master regulator genes of severe persistent asthma in children (LRRC23, TMEM231, CAPS, PTPRC, and FYB); and (3) master regulator genes of mild/moderate persistent asthma in children and adults (C1orf38 and FMNL1). The identified master regulators were statistically inferred to causally regulate the expression of downstream genes that modulate ciliary function and inflammatory response to influence asthma.RESULTSNasal gene signatures for severe persistent asthma and for mild/moderate persistent asthma were identified; both were found to be enriched in coexpression network modules for ciliary function and inflammatory response. By applying probabilistic causal methods to these gene signatures and validation testing in independent cohorts, we identified (1) a master regulator gene common to asthma across severity and ages (FOXJ1); (2) master regulator genes of severe persistent asthma in children (LRRC23, TMEM231, CAPS, PTPRC, and FYB); and (3) master regulator genes of mild/moderate persistent asthma in children and adults (C1orf38 and FMNL1). The identified master regulators were statistically inferred to causally regulate the expression of downstream genes that modulate ciliary function and inflammatory response to influence asthma.The identified master regulator genes of asthma provide a novel path forward to further uncovering asthma mechanisms and therapy.CONCLUSIONThe identified master regulator genes of asthma provide a novel path forward to further uncovering asthma mechanisms and therapy. BackgroundNasal transcriptomics can provide an accessible window into asthma pathobiology.ObjectiveOur goal was to move beyond gene signatures of asthma to identify master regulator genes that causally regulate genes associated with asthma phenotypes.MethodsWe recruited 156 children with severe persistent asthma and controls for nasal transcriptome profiling and applied network-based and probabilistic causal methods to identify severe asthma genes and their master regulators. We then took the same approach in an independent cohort of 190 adults with mild/moderate asthma and controls to identify mild/moderate asthma genes and their master regulators. Comparative analysis of the master regulator genes followed by validation testing in independent children with severe asthma (n = 21) and mild/moderate asthma (n = 154) was then performed.ResultsNasal gene signatures for severe persistent asthma and for mild/moderate persistent asthma were identified; both were found to be enriched in coexpression network modules for ciliary function and inflammatory response. By applying probabilistic causal methods to these gene signatures and validation testing in independent cohorts, we identified (1) a master regulator gene common to asthma across severity and ages (FOXJ1); (2) master regulator genes of severe persistent asthma in children (LRRC23, TMEM231, CAPS, PTPRC, and FYB); and (3) master regulator genes of mild/moderate persistent asthma in children and adults (C1orf38 and FMNL1). The identified master regulators were statistically inferred to causally regulate the expression of downstream genes that modulate ciliary function and inflammatory response to influence asthma.ConclusionThe identified master regulator genes of asthma provide a novel path forward to further uncovering asthma mechanisms and therapy. |
| Author | Chun, Yoojin Schadt, Eric E. Do, Anh N. Raby, Benjamin A. Grishin, Alexander Grishina, Galina Weiss, Scott T. Rogers, Angela J. Bunyavanich, Supinda Vicencio, Alfin |
| AuthorAffiliation | 6 Division of Pulmonary Medicine, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY, USA 1 Icahn Institute for Genomics and Multiscale Biology and Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA 2 Division of Allergy & Immunology, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY, USA 4 Division of Pulmonary Medicine, Children’s Hospital Boston, Boston, MA, USA 5 Channing Division of Network Medicine and Division of Pulmonary and Critical Care Medicine, Brigham & Women’s Hospital, and Harvard Medical School, Boston, MA, USA 3 Division of Pulmonary and Critical Care Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA |
| AuthorAffiliation_xml | – name: 3 Division of Pulmonary and Critical Care Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA – name: 4 Division of Pulmonary Medicine, Children’s Hospital Boston, Boston, MA, USA – name: 5 Channing Division of Network Medicine and Division of Pulmonary and Critical Care Medicine, Brigham & Women’s Hospital, and Harvard Medical School, Boston, MA, USA – name: 1 Icahn Institute for Genomics and Multiscale Biology and Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA – name: 2 Division of Allergy & Immunology, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY, USA – name: 6 Division of Pulmonary Medicine, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY, USA |
| Author_xml | – sequence: 1 givenname: Anh N. surname: Do fullname: Do, Anh N. organization: Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 2 givenname: Yoojin surname: Chun fullname: Chun, Yoojin organization: Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 3 givenname: Galina surname: Grishina fullname: Grishina, Galina organization: Division of Allergy and Immunology, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 4 givenname: Alexander surname: Grishin fullname: Grishin, Alexander organization: Division of Allergy and Immunology, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 5 givenname: Angela J. surname: Rogers fullname: Rogers, Angela J. organization: Division of Pulmonary and Critical Care Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, Calif – sequence: 6 givenname: Benjamin A. surname: Raby fullname: Raby, Benjamin A. organization: Division of Pulmonary Medicine, Children’s Hospital Boston, Boston, Mass – sequence: 7 givenname: Scott T. surname: Weiss fullname: Weiss, Scott T. organization: Channing Division of Network Medicine, Brigham and Women’s Hospital, and Harvard Medical School, Boston, Mass – sequence: 8 givenname: Alfin surname: Vicencio fullname: Vicencio, Alfin organization: Division of Pulmonary Medicine, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 9 givenname: Eric E. surname: Schadt fullname: Schadt, Eric E. organization: Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 10 givenname: Supinda orcidid: 0000-0001-6108-439X surname: Bunyavanich fullname: Bunyavanich, Supinda email: supinda@post.harvard.edu organization: Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32828590$$D View this record in MEDLINE/PubMed |
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| Snippet | Nasal transcriptomics can provide an accessible window into asthma pathobiology.
Our goal was to move beyond gene signatures of asthma to identify master... BackgroundNasal transcriptomics can provide an accessible window into asthma pathobiology.ObjectiveOur goal was to move beyond gene signatures of asthma to... Nasal transcriptomics can provide an accessible window into asthma pathobiology.BACKGROUNDNasal transcriptomics can provide an accessible window into asthma... Network study of nasal transcriptome profiles from multiple human cohorts identified nasal gene signatures for severe persistent asthma, mild/moderate... |
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| SubjectTerms | Adolescent Age Asthma Asthma - genetics Child Children Cohort Studies Comparative analysis Digital Object Identifier Disease Family medical history Female Forkhead Transcription Factors - genetics Formins - genetics Gene expression Gene Expression Profiling Humans Inflammation Intracellular Signaling Peptides and Proteins - genetics Male master regulator mild persistent asthma Models, Statistical moderate persistent asthma nasal network Nose - physiology Phenotype Phenotypes probabilistic causal network Quality control severe persistent asthma Spirometry Transcriptome Transcriptomes |
| Title | Network study of nasal transcriptome profiles reveals master regulator genes of asthma |
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