Vitamin D related genes in lung development and asthma pathogenesis
Background Poor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that in utero changes related to vitamin D responsive genes might play a crucial role in later disease susceptibility. We hypothesized that vitamin D pathway genes are developmentally active in the...
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| Published in | BMC medical genomics Vol. 6; no. 1; p. 47 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
BioMed Central
05.11.2013
BioMed Central Ltd |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1755-8794 1755-8794 |
| DOI | 10.1186/1755-8794-6-47 |
Cover
| Abstract | Background
Poor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that
in utero
changes related to vitamin D responsive genes might play a crucial role in later disease susceptibility. We hypothesized that vitamin D pathway genes are developmentally active in the fetal lung and that these developmental genes would be associated with asthma susceptibility and regulation in asthma.
Methods
Vitamin D pathway genes were derived from PubMed and Gene Ontology surveys. Principal component analysis was used to identify characteristic lung development genes.
Results
Vitamin D regulated genes were markedly over-represented in normal human (odds ratio OR 2.15, 95% confidence interval CI: 1.69-2.74) and mouse (OR 2.68, 95% CI: 2.12-3.39) developing lung transcriptomes. 38 vitamin D pathway genes were in both developing lung transcriptomes with >63% of genes more highly expressed in the later than earlier stages of development. In immortalized B-cells derived from 95 asthmatics and their unaffected siblings, 12 of the 38 (31.6%) vitamin D pathway lung development genes were significantly differentially expressed (OR 3.00, 95% CI: 1.43-6.21), whereas 11 (29%) genes were significantly differentially expressed in 43 control versus vitamin D treated immortalized B-cells from Childhood Asthma Management Program subjects (OR 2.62, 95% CI: 1.22-5.50). 4 genes,
LAMP3
,
PIP5K1B
,
SCARB2
and
TXNIP
were identified in both groups; each displays significant biologic plausibility for a role in asthma.
Conclusions
Our findings demonstrate a significant association between early lung development and asthma–related phenotypes for vitamin D pathway genes, supporting a genomic mechanistic basis for the epidemiologic observations relating maternal vitamin D intake and childhood asthma susceptibility. |
|---|---|
| AbstractList | Doc number: 47 Abstract Background: Poor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that in utero changes related to vitamin D responsive genes might play a crucial role in later disease susceptibility. We hypothesized that vitamin D pathway genes are developmentally active in the fetal lung and that these developmental genes would be associated with asthma susceptibility and regulation in asthma. Methods: Vitamin D pathway genes were derived from PubMed and Gene Ontology surveys. Principal component analysis was used to identify characteristic lung development genes. Results: Vitamin D regulated genes were markedly over-represented in normal human (odds ratio OR 2.15, 95% confidence interval CI: 1.69-2.74) and mouse (OR 2.68, 95% CI: 2.12-3.39) developing lung transcriptomes. 38 vitamin D pathway genes were in both developing lung transcriptomes with >63% of genes more highly expressed in the later than earlier stages of development. In immortalized B-cells derived from 95 asthmatics and their unaffected siblings, 12 of the 38 (31.6%) vitamin D pathway lung development genes were significantly differentially expressed (OR 3.00, 95% CI: 1.43-6.21), whereas 11 (29%) genes were significantly differentially expressed in 43 control versus vitamin D treated immortalized B-cells from Childhood Asthma Management Program subjects (OR 2.62, 95% CI: 1.22-5.50). 4 genes, LAMP3 , PIP5K1B , SCARB2 and TXNIP were identified in both groups; each displays significant biologic plausibility for a role in asthma. Conclusions: Our findings demonstrate a significant association between early lung development and asthma-related phenotypes for vitamin D pathway genes, supporting a genomic mechanistic basis for the epidemiologic observations relating maternal vitamin D intake and childhood asthma susceptibility. Poor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that in utero changes related to vitamin D responsive genes might play a crucial role in later disease susceptibility. We hypothesized that vitamin D pathway genes are developmentally active in the fetal lung and that these developmental genes would be associated with asthma susceptibility and regulation in asthma.BACKGROUNDPoor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that in utero changes related to vitamin D responsive genes might play a crucial role in later disease susceptibility. We hypothesized that vitamin D pathway genes are developmentally active in the fetal lung and that these developmental genes would be associated with asthma susceptibility and regulation in asthma.Vitamin D pathway genes were derived from PubMed and Gene Ontology surveys. Principal component analysis was used to identify characteristic lung development genes.METHODSVitamin D pathway genes were derived from PubMed and Gene Ontology surveys. Principal component analysis was used to identify characteristic lung development genes.Vitamin D regulated genes were markedly over-represented in normal human (odds ratio OR 2.15, 95% confidence interval CI: 1.69-2.74) and mouse (OR 2.68, 95% CI: 2.12-3.39) developing lung transcriptomes. 38 vitamin D pathway genes were in both developing lung transcriptomes with >63% of genes more highly expressed in the later than earlier stages of development. In immortalized B-cells derived from 95 asthmatics and their unaffected siblings, 12 of the 38 (31.6%) vitamin D pathway lung development genes were significantly differentially expressed (OR 3.00, 95% CI: 1.43-6.21), whereas 11 (29%) genes were significantly differentially expressed in 43 control versus vitamin D treated immortalized B-cells from Childhood Asthma Management Program subjects (OR 2.62, 95% CI: 1.22-5.50). 4 genes, LAMP3, PIP5K1B, SCARB2 and TXNIP were identified in both groups; each displays significant biologic plausibility for a role in asthma.RESULTSVitamin D regulated genes were markedly over-represented in normal human (odds ratio OR 2.15, 95% confidence interval CI: 1.69-2.74) and mouse (OR 2.68, 95% CI: 2.12-3.39) developing lung transcriptomes. 38 vitamin D pathway genes were in both developing lung transcriptomes with >63% of genes more highly expressed in the later than earlier stages of development. In immortalized B-cells derived from 95 asthmatics and their unaffected siblings, 12 of the 38 (31.6%) vitamin D pathway lung development genes were significantly differentially expressed (OR 3.00, 95% CI: 1.43-6.21), whereas 11 (29%) genes were significantly differentially expressed in 43 control versus vitamin D treated immortalized B-cells from Childhood Asthma Management Program subjects (OR 2.62, 95% CI: 1.22-5.50). 4 genes, LAMP3, PIP5K1B, SCARB2 and TXNIP were identified in both groups; each displays significant biologic plausibility for a role in asthma.Our findings demonstrate a significant association between early lung development and asthma-related phenotypes for vitamin D pathway genes, supporting a genomic mechanistic basis for the epidemiologic observations relating maternal vitamin D intake and childhood asthma susceptibility.CONCLUSIONSOur findings demonstrate a significant association between early lung development and asthma-related phenotypes for vitamin D pathway genes, supporting a genomic mechanistic basis for the epidemiologic observations relating maternal vitamin D intake and childhood asthma susceptibility. Poor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that in utero changes related to vitamin D responsive genes might play a crucial role in later disease susceptibility. We hypothesized that vitamin D pathway genes are developmentally active in the fetal lung and that these developmental genes would be associated with asthma susceptibility and regulation in asthma. Vitamin D pathway genes were derived from PubMed and Gene Ontology surveys. Principal component analysis was used to identify characteristic lung development genes. Vitamin D regulated genes were markedly over-represented in normal human (odds ratio OR 2.15, 95% confidence interval CI: 1.69-2.74) and mouse (OR 2.68, 95% CI: 2.12-3.39) developing lung transcriptomes. 38 vitamin D pathway genes were in both developing lung transcriptomes with >63% of genes more highly expressed in the later than earlier stages of development. In immortalized B-cells derived from 95 asthmatics and their unaffected siblings, 12 of the 38 (31.6%) vitamin D pathway lung development genes were significantly differentially expressed (OR 3.00, 95% CI: 1.43-6.21), whereas 11 (29%) genes were significantly differentially expressed in 43 control versus vitamin D treated immortalized B-cells from Childhood Asthma Management Program subjects (OR 2.62, 95% CI: 1.22-5.50). 4 genes, LAMP3, PIP5K1B, SCARB2 and TXNIP were identified in both groups; each displays significant biologic plausibility for a role in asthma. Our findings demonstrate a significant association between early lung development and asthma-related phenotypes for vitamin D pathway genes, supporting a genomic mechanistic basis for the epidemiologic observations relating maternal vitamin D intake and childhood asthma susceptibility. Poor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that in utero changes related to vitamin D responsive genes might play a crucial role in later disease susceptibility. We hypothesized that vitamin D pathway genes are developmentally active in the fetal lung and that these developmental genes would be associated with asthma susceptibility and regulation in asthma. Vitamin D pathway genes were derived from PubMed and Gene Ontology surveys. Principal component analysis was used to identify characteristic lung development genes. Vitamin D regulated genes were markedly over-represented in normal human (odds ratio OR 2.15, 95% confidence interval CI: 1.69-2.74) and mouse (OR 2.68, 95% CI: 2.12-3.39) developing lung transcriptomes. 38 vitamin D pathway genes were in both developing lung transcriptomes with >63% of genes more highly expressed in the later than earlier stages of development. In immortalized B-cells derived from 95 asthmatics and their unaffected siblings, 12 of the 38 (31.6%) vitamin D pathway lung development genes were significantly differentially expressed (OR 3.00, 95% CI: 1.43-6.21), whereas 11 (29%) genes were significantly differentially expressed in 43 control versus vitamin D treated immortalized B-cells from Childhood Asthma Management Program subjects (OR 2.62, 95% CI: 1.22-5.50). 4 genes, LAMP3, PIP5K1B, SCARB2 and TXNIP were identified in both groups; each displays significant biologic plausibility for a role in asthma. Our findings demonstrate a significant association between early lung development and asthma-related phenotypes for vitamin D pathway genes, supporting a genomic mechanistic basis for the epidemiologic observations relating maternal vitamin D intake and childhood asthma susceptibility. Background: Poor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that in utero changes related to vitamin D responsive genes might play a crucial role in later disease susceptibility. We hypothesized that vitamin D pathway genes are developmentally active in the fetal lung and that these developmental genes would be associated with asthma susceptibility and regulation in asthma. Methods: Vitamin D pathway genes were derived from PubMed and Gene Ontology surveys. Principal component analysis was used to identify characteristic lung development genes. Results: Vitamin D regulated genes were markedly over-represented in normal human (odds ratio OR 2.15, 95% confidence interval CI: 1.69-2.74) and mouse (OR 2.68, 95% CI: 2.12-3.39) developing lung transcriptomes. 38 vitamin D pathway genes were in both developing lung transcriptomes with >63% of genes more highly expressed in the later than earlier stages of development. In immortalized B-cells derived from 95 asthmatics and their unaffected siblings, 12 of the 38 (31.6%) vitamin D pathway lung development genes were significantly differentially expressed (OR 3.00, 95% CI: 1.43-6.21), whereas 11 (29%) genes were significantly differentially expressed in 43 control versus vitamin D treated immortalized B-cells from Childhood Asthma Management Program subjects (OR 2.62, 95% CI: 1.22-5.50). 4 genes, LAMP3, PIP5K1B, SCARB2 and TXNIP were identified in both groups; each displays significant biologic plausibility for a role in asthma. Conclusions: Our findings demonstrate a significant association between early lung development and asthma-related phenotypes for vitamin D pathway genes, supporting a genomic mechanistic basis for the epidemiologic observations relating maternal vitamin D intake and childhood asthma susceptibility. Background Poor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that in utero changes related to vitamin D responsive genes might play a crucial role in later disease susceptibility. We hypothesized that vitamin D pathway genes are developmentally active in the fetal lung and that these developmental genes would be associated with asthma susceptibility and regulation in asthma. Methods Vitamin D pathway genes were derived from PubMed and Gene Ontology surveys. Principal component analysis was used to identify characteristic lung development genes. Results Vitamin D regulated genes were markedly over-represented in normal human (odds ratio OR 2.15, 95% confidence interval CI: 1.69-2.74) and mouse (OR 2.68, 95% CI: 2.12-3.39) developing lung transcriptomes. 38 vitamin D pathway genes were in both developing lung transcriptomes with >63% of genes more highly expressed in the later than earlier stages of development. In immortalized B-cells derived from 95 asthmatics and their unaffected siblings, 12 of the 38 (31.6%) vitamin D pathway lung development genes were significantly differentially expressed (OR 3.00, 95% CI: 1.43-6.21), whereas 11 (29%) genes were significantly differentially expressed in 43 control versus vitamin D treated immortalized B-cells from Childhood Asthma Management Program subjects (OR 2.62, 95% CI: 1.22-5.50). 4 genes, LAMP3 , PIP5K1B , SCARB2 and TXNIP were identified in both groups; each displays significant biologic plausibility for a role in asthma. Conclusions Our findings demonstrate a significant association between early lung development and asthma–related phenotypes for vitamin D pathway genes, supporting a genomic mechanistic basis for the epidemiologic observations relating maternal vitamin D intake and childhood asthma susceptibility. Background Poor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that in utero changes related to vitamin D responsive genes might play a crucial role in later disease susceptibility. We hypothesized that vitamin D pathway genes are developmentally active in the fetal lung and that these developmental genes would be associated with asthma susceptibility and regulation in asthma. Methods Vitamin D pathway genes were derived from PubMed and Gene Ontology surveys. Principal component analysis was used to identify characteristic lung development genes. Results Vitamin D regulated genes were markedly over-represented in normal human (odds ratio OR 2.15, 95% confidence interval CI: 1.69-2.74) and mouse (OR 2.68, 95% CI: 2.12-3.39) developing lung transcriptomes. 38 vitamin D pathway genes were in both developing lung transcriptomes with >63% of genes more highly expressed in the later than earlier stages of development. In immortalized B-cells derived from 95 asthmatics and their unaffected siblings, 12 of the 38 (31.6%) vitamin D pathway lung development genes were significantly differentially expressed (OR 3.00, 95% CI: 1.43-6.21), whereas 11 (29%) genes were significantly differentially expressed in 43 control versus vitamin D treated immortalized B-cells from Childhood Asthma Management Program subjects (OR 2.62, 95% CI: 1.22-5.50). 4 genes, LAMP3, PIP5K1B, SCARB2 and TXNIP were identified in both groups; each displays significant biologic plausibility for a role in asthma. Conclusions Our findings demonstrate a significant association between early lung development and asthma-related phenotypes for vitamin D pathway genes, supporting a genomic mechanistic basis for the epidemiologic observations relating maternal vitamin D intake and childhood asthma susceptibility. Keywords: Vitamin D, Cholecalciferol, Lung development, Asthma, Fetal programming |
| ArticleNumber | 47 |
| Audience | Academic |
| Author | Gaedigk, Roger Klanderman, Barbara Tantisira, Kelan G Qiu, Weiliang Niu, Simin Sharma, Sunita Leeder, James S Kho, Alvin T Weiss, Scott T Anderson, Chris |
| AuthorAffiliation | 2 Harvard Medical School, Boston, MA, USA 8 Channing Division of Network Medicine, Brigham and Women’s Hospital and Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA 9 Division of Pediatric Clinical Pharmacology and Medical Toxicology, Children’s Mercy Hospital and Clinics, 2401 Gilham Road, Kansas City, MO 64108, USA 10 Department of Microbiology and Immunology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA 3 Channing Division of Network Medicine, Brigham and Women’s Hospital, 181 Longwood Avenue, Boston, MA 02115, USA 5 Children’s Mercy Hospital, Kansas City, MO, USA 6 Partners Health Care Center for Personalized Genetic Medicine, Boston, MA, USA 7 University of Rochester Medical Center, Rochester, NY, USA 1 Children’s Hospital Informatics Program, Boston Children’s Hospital, 320 Longwood Avenue, Boston, MA 02115, USA 4 Pulmonary Division, Brigham and Women’s Hospital, Boston, MA, USA |
| AuthorAffiliation_xml | – name: 4 Pulmonary Division, Brigham and Women’s Hospital, Boston, MA, USA – name: 9 Division of Pediatric Clinical Pharmacology and Medical Toxicology, Children’s Mercy Hospital and Clinics, 2401 Gilham Road, Kansas City, MO 64108, USA – name: 10 Department of Microbiology and Immunology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA – name: 3 Channing Division of Network Medicine, Brigham and Women’s Hospital, 181 Longwood Avenue, Boston, MA 02115, USA – name: 2 Harvard Medical School, Boston, MA, USA – name: 5 Children’s Mercy Hospital, Kansas City, MO, USA – name: 6 Partners Health Care Center for Personalized Genetic Medicine, Boston, MA, USA – name: 7 University of Rochester Medical Center, Rochester, NY, USA – name: 8 Channing Division of Network Medicine, Brigham and Women’s Hospital and Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA – name: 1 Children’s Hospital Informatics Program, Boston Children’s Hospital, 320 Longwood Avenue, Boston, MA 02115, USA |
| Author_xml | – sequence: 1 givenname: Alvin T surname: Kho fullname: Kho, Alvin T organization: Children’s Hospital Informatics Program, Boston Children’s Hospital, Harvard Medical School – sequence: 2 givenname: Sunita surname: Sharma fullname: Sharma, Sunita organization: Harvard Medical School, Channing Division of Network Medicine, Brigham and Women’s Hospital, Pulmonary Division, Brigham and Women’s Hospital, Channing Division of Network Medicine, Brigham and Women’s Hospital and Harvard Medical School – sequence: 3 givenname: Weiliang surname: Qiu fullname: Qiu, Weiliang organization: Channing Division of Network Medicine, Brigham and Women’s Hospital, Channing Division of Network Medicine, Brigham and Women’s Hospital and Harvard Medical School – sequence: 4 givenname: Roger surname: Gaedigk fullname: Gaedigk, Roger organization: Children’s Mercy Hospital, Division of Pediatric Clinical Pharmacology and Medical Toxicology, Children’s Mercy Hospital and Clinics – sequence: 5 givenname: Barbara surname: Klanderman fullname: Klanderman, Barbara organization: Channing Division of Network Medicine, Brigham and Women’s Hospital, Channing Division of Network Medicine, Brigham and Women’s Hospital and Harvard Medical School – sequence: 6 givenname: Simin surname: Niu fullname: Niu, Simin organization: Channing Division of Network Medicine, Brigham and Women’s Hospital, Channing Division of Network Medicine, Brigham and Women’s Hospital and Harvard Medical School – sequence: 7 givenname: Chris surname: Anderson fullname: Anderson, Chris organization: University of Rochester Medical Center, Department of Microbiology and Immunology, University of Rochester Medical Center – sequence: 8 givenname: James S surname: Leeder fullname: Leeder, James S organization: Children’s Mercy Hospital, Division of Pediatric Clinical Pharmacology and Medical Toxicology, Children’s Mercy Hospital and Clinics – sequence: 9 givenname: Scott T surname: Weiss fullname: Weiss, Scott T organization: Harvard Medical School, Channing Division of Network Medicine, Brigham and Women’s Hospital, Partners Health Care Center for Personalized Genetic Medicine, Channing Division of Network Medicine, Brigham and Women’s Hospital and Harvard Medical School – sequence: 10 givenname: Kelan G surname: Tantisira fullname: Tantisira, Kelan G email: kelan.tantisira@channing.harvard.edu organization: Harvard Medical School, Channing Division of Network Medicine, Brigham and Women’s Hospital, Pulmonary Division, Brigham and Women’s Hospital, Channing Division of Network Medicine, Brigham and Women’s Hospital and Harvard Medical School |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24188128$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | Kho et al.; licensee BioMed Central Ltd. 2013 This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. COPYRIGHT 2013 BioMed Central Ltd. 2013 Kho et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright © 2013 Kho et al.; licensee BioMed Central Ltd. 2013 Kho et al.; licensee BioMed Central Ltd. |
| Copyright_xml | – notice: Kho et al.; licensee BioMed Central Ltd. 2013 This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. – notice: COPYRIGHT 2013 BioMed Central Ltd. – notice: 2013 Kho et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. – notice: Copyright © 2013 Kho et al.; licensee BioMed Central Ltd. 2013 Kho et al.; licensee BioMed Central Ltd. |
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| DOI | 10.1186/1755-8794-6-47 |
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| Keywords | Lung development Vitamin D Cholecalciferol Fetal programming Asthma |
| Language | English |
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| Snippet | Background
Poor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that
in utero
changes related to vitamin D responsive... Poor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that in utero changes related to vitamin D responsive genes might... Background Poor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that in utero changes related to vitamin D responsive... Doc number: 47 Abstract Background: Poor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that in utero changes related... Background: Poor maternal vitamin D intake is a risk factor for subsequent childhood asthma, suggesting that in utero changes related to vitamin D responsive... |
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| SubjectTerms | Alfacalcidol Animals Asthma Asthma - etiology Asthma - genetics Asthma in children Bioinformatic and algorithmical studies Biomedical and Life Sciences Biomedicine Calcifediol Cell Line Child Children & youth Colleges & universities Computational Biology Confidence intervals Disease Disease susceptibility Gene Expression Gene Expression Profiling Genes Genetic aspects Genetic Predisposition to Disease - genetics Genomes Hospitals Human Genetics Humans Hypotheses Laboratory animals Lung - growth & development Mice Microarrays Ontology Pediatrics Physiological aspects Pregnancy Principal components analysis Research Article Risk factors Vitamin D Vitamin D - metabolism Vitamin deficiency Womens health World Asthma Day 2014: recent insights into asthma Writing |
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| Title | Vitamin D related genes in lung development and asthma pathogenesis |
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