Epigenome-wide analysis of long-term air pollution exposure and DNA methylation in monocytes: results from the Multi-Ethnic Study of Atherosclerosis
Air pollution might affect atherosclerosis through DNA methylation changes in cells crucial to atherosclerosis, such as monocytes. We conducted an epigenome-wide study of DNA methylation in CD14+ monocytes and long-term ambient air pollution exposure in adults participating in the Multi-Ethnic Study...
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| Published in | Epigenetics Vol. 17; no. 3; pp. 297 - 313 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Taylor & Francis
04.03.2022
Taylor & Francis Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1559-2294 1559-2308 1559-2308 |
| DOI | 10.1080/15592294.2021.1900028 |
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| Abstract | Air pollution might affect atherosclerosis through DNA methylation changes in cells crucial to atherosclerosis, such as monocytes. We conducted an epigenome-wide study of DNA methylation in CD14+ monocytes and long-term ambient air pollution exposure in adults participating in the Multi-Ethnic Study of Atherosclerosis (MESA). We also assessed the association between differentially methylated signals and cis-gene expression. Using spatiotemporal models, one-year average concentrations of outdoor fine particulate matter (PM
2.5
) and oxides of nitrogen (NO
X
) were estimated at participants' homes. We assessed DNA methylation and gene expression using Illumina 450k and HumanHT-12 v4 Expression BeadChips, respectively (n = 1,207). We used bump hunting and site-specific approaches to identify differentially methylated signals (false discovery rate of 0.05) and used linear models to assess associations between differentially methylated signals and cis-gene expression. Four differentially methylated regions (DMRs) located on chromosomes 5, 6, 7, and 16 (within or near SDHAP3, ZFP57, HOXA5, and PRM1, respectively) were associated with PM
2.5
. The DMRs on chromosomes 5 and 6 also associated with NO
X
. The DMR on chromosome 5 had the smallest p-value for both PM
2.5
(p = 1.4×10
−6
) and NO
X
(p = 7.7×10
−6
). Three differentially methylated CpGs were identified for PM
2.5
, and cg05926640 (near TOMM20) had the smallest p-value (p = 5.6×10
−8
). NO
X
significantly associated with cg11756214 within ZNF347 (p = 5.6×10
−8
). Several differentially methylated signals were also associated with cis-gene expression. The DMR located on chromosome 7 was associated with the expression of HOXA5, HOXA9, and HOXA10. The DMRs located on chromosomes 5 and 16 were associated with expression of MRPL36 and DEXI, respectively. The CpG cg05926640 was associated with expression of ARID4B, IRF2BP2, and TOMM20. We identified differential DNA methylation in monocytes associated with long-term air pollution exposure. Methylation signals associated with gene expression might help explain how air pollution contributes to cardiovascular disease. |
|---|---|
| AbstractList | Air pollution might affect atherosclerosis through DNA methylation changes in cells crucial to atherosclerosis, such as monocytes. We conducted an epigenome-wide study of DNA methylation in CD14+ monocytes and long-term ambient air pollution exposure in adults participating in the Multi-Ethnic Study of Atherosclerosis (MESA). We also assessed the association between differentially methylated signals and
cis
-gene expression. Using spatiotemporal models, one-year average concentrations of outdoor fine particulate matter (PM
2.5
) and oxides of nitrogen (NO
X
) were estimated at participants’ homes. We assessed DNA methylation and gene expression using Illumina 450k and HumanHT-12 v4 Expression BeadChips, respectively (n = 1,207). We used bump hunting and site-specific approaches to identify differentially methylated signals (false discovery rate of 0.05) and used linear models to assess associations between differentially methylated signals and
cis
-gene expression. Four differentially methylated regions (DMRs) located on chromosomes 5, 6, 7, and 16 (within or near
SDHAP3, ZFP57, HOXA5
, and
PRM1
, respectively) were associated with PM
2.5
. The DMRs on chromosomes 5 and 6 also associated with NO
X
. The DMR on chromosome 5 had the smallest p-value for both PM
2.5
(p = 1.4×10
−6
) and NO
X
(p = 7.7×10
−6
). Three differentially methylated CpGs were identified for PM
2.5
, and cg05926640 (near
TOMM20
) had the smallest p-value (p = 5.6×10
−8
). NO
X
significantly associated with cg11756214 within
ZNF347
(p = 5.6×10
−8
). Several differentially methylated signals were also associated with
cis
-gene expression. The DMR located on chromosome 7 was associated with the expression of
HOXA5, HOXA9
, and
HOXA10
. The DMRs located on chromosomes 5 and 16 were associated with expression of
MRPL36
and
DEXI
, respectively. The CpG cg05926640 was associated with expression of
ARID4B, IRF2BP2
, and
TOMM20
. We identified differential DNA methylation in monocytes associated with long-term air pollution exposure. Methylation signals associated with gene expression might help explain how air pollution contributes to cardiovascular disease. Air pollution might affect atherosclerosis through DNA methylation changes in cells crucial to atherosclerosis, such as monocytes. We conducted an epigenome-wide study of DNA methylation in CD14+ monocytes and long-term ambient air pollution exposure in adults participating in the Multi-Ethnic Study of Atherosclerosis (MESA). We also assessed the association between differentially methylated signals and cis-gene expression. Using spatiotemporal models, one-year average concentrations of outdoor fine particulate matter (PM 2.5 ) and oxides of nitrogen (NO X ) were estimated at participants' homes. We assessed DNA methylation and gene expression using Illumina 450k and HumanHT-12 v4 Expression BeadChips, respectively (n = 1,207). We used bump hunting and site-specific approaches to identify differentially methylated signals (false discovery rate of 0.05) and used linear models to assess associations between differentially methylated signals and cis-gene expression. Four differentially methylated regions (DMRs) located on chromosomes 5, 6, 7, and 16 (within or near SDHAP3, ZFP57, HOXA5, and PRM1, respectively) were associated with PM 2.5 . The DMRs on chromosomes 5 and 6 also associated with NO X . The DMR on chromosome 5 had the smallest p-value for both PM 2.5 (p = 1.4×10 −6 ) and NO X (p = 7.7×10 −6 ). Three differentially methylated CpGs were identified for PM 2.5 , and cg05926640 (near TOMM20) had the smallest p-value (p = 5.6×10 −8 ). NO X significantly associated with cg11756214 within ZNF347 (p = 5.6×10 −8 ). Several differentially methylated signals were also associated with cis-gene expression. The DMR located on chromosome 7 was associated with the expression of HOXA5, HOXA9, and HOXA10. The DMRs located on chromosomes 5 and 16 were associated with expression of MRPL36 and DEXI, respectively. The CpG cg05926640 was associated with expression of ARID4B, IRF2BP2, and TOMM20. We identified differential DNA methylation in monocytes associated with long-term air pollution exposure. Methylation signals associated with gene expression might help explain how air pollution contributes to cardiovascular disease. Air pollution might affect atherosclerosis through DNA methylation changes in cells crucial to atherosclerosis, such as monocytes. We conducted an epigenome-wide study of DNA methylation in CD14+ monocytes and long-term ambient air pollution exposure in adults participating in the Multi-Ethnic Study of Atherosclerosis (MESA). We also assessed the association between differentially methylated signals and cis-gene expression. Using spatiotemporal models, one-year average concentrations of outdoor fine particulate matter (PM2.5) and oxides of nitrogen (NOX) were estimated at participants' homes. We assessed DNA methylation and gene expression using Illumina 450k and HumanHT-12 v4 Expression BeadChips, respectively (n = 1,207). We used bump hunting and site-specific approaches to identify differentially methylated signals (false discovery rate of 0.05) and used linear models to assess associations between differentially methylated signals and cis-gene expression. Four differentially methylated regions (DMRs) located on chromosomes 5, 6, 7, and 16 (within or near SDHAP3, ZFP57, HOXA5, and PRM1, respectively) were associated with PM2.5. The DMRs on chromosomes 5 and 6 also associated with NOX. The DMR on chromosome 5 had the smallest p-value for both PM2.5 (p = 1.4×10-6) and NOX (p = 7.7×10-6). Three differentially methylated CpGs were identified for PM2.5, and cg05926640 (near TOMM20) had the smallest p-value (p = 5.6×10-8). NOX significantly associated with cg11756214 within ZNF347 (p = 5.6×10-8). Several differentially methylated signals were also associated with cis-gene expression. The DMR located on chromosome 7 was associated with the expression of HOXA5, HOXA9, and HOXA10. The DMRs located on chromosomes 5 and 16 were associated with expression of MRPL36 and DEXI, respectively. The CpG cg05926640 was associated with expression of ARID4B, IRF2BP2, and TOMM20. We identified differential DNA methylation in monocytes associated with long-term air pollution exposure. Methylation signals associated with gene expression might help explain how air pollution contributes to cardiovascular disease.Air pollution might affect atherosclerosis through DNA methylation changes in cells crucial to atherosclerosis, such as monocytes. We conducted an epigenome-wide study of DNA methylation in CD14+ monocytes and long-term ambient air pollution exposure in adults participating in the Multi-Ethnic Study of Atherosclerosis (MESA). We also assessed the association between differentially methylated signals and cis-gene expression. Using spatiotemporal models, one-year average concentrations of outdoor fine particulate matter (PM2.5) and oxides of nitrogen (NOX) were estimated at participants' homes. We assessed DNA methylation and gene expression using Illumina 450k and HumanHT-12 v4 Expression BeadChips, respectively (n = 1,207). We used bump hunting and site-specific approaches to identify differentially methylated signals (false discovery rate of 0.05) and used linear models to assess associations between differentially methylated signals and cis-gene expression. Four differentially methylated regions (DMRs) located on chromosomes 5, 6, 7, and 16 (within or near SDHAP3, ZFP57, HOXA5, and PRM1, respectively) were associated with PM2.5. The DMRs on chromosomes 5 and 6 also associated with NOX. The DMR on chromosome 5 had the smallest p-value for both PM2.5 (p = 1.4×10-6) and NOX (p = 7.7×10-6). Three differentially methylated CpGs were identified for PM2.5, and cg05926640 (near TOMM20) had the smallest p-value (p = 5.6×10-8). NOX significantly associated with cg11756214 within ZNF347 (p = 5.6×10-8). Several differentially methylated signals were also associated with cis-gene expression. The DMR located on chromosome 7 was associated with the expression of HOXA5, HOXA9, and HOXA10. The DMRs located on chromosomes 5 and 16 were associated with expression of MRPL36 and DEXI, respectively. The CpG cg05926640 was associated with expression of ARID4B, IRF2BP2, and TOMM20. We identified differential DNA methylation in monocytes associated with long-term air pollution exposure. Methylation signals associated with gene expression might help explain how air pollution contributes to cardiovascular disease. Air pollution might affect atherosclerosis through DNA methylation changes in cells crucial to atherosclerosis, such as monocytes. We conducted an epigenome-wide study of DNA methylation in CD14+ monocytes and long-term ambient air pollution exposure in adults participating in the Multi-Ethnic Study of Atherosclerosis (MESA). We also assessed the association between differentially methylated signals and cis-gene expression. Using spatiotemporal models, one-year average concentrations of outdoor fine particulate matter (PM2.5) and oxides of nitrogen (NOX) were estimated at participants’ homes. We assessed DNA methylation and gene expression using Illumina 450k and HumanHT-12 v4 Expression BeadChips, respectively (n = 1,207). We used bump hunting and site-specific approaches to identify differentially methylated signals (false discovery rate of 0.05) and used linear models to assess associations between differentially methylated signals and cis-gene expression. Four differentially methylated regions (DMRs) located on chromosomes 5, 6, 7, and 16 (within or near SDHAP3, ZFP57, HOXA5, and PRM1, respectively) were associated with PM2.5. The DMRs on chromosomes 5 and 6 also associated with NOX. The DMR on chromosome 5 had the smallest p-value for both PM2.5 (p = 1.4×10−6) and NOX (p = 7.7×10−6). Three differentially methylated CpGs were identified for PM2.5, and cg05926640 (near TOMM20) had the smallest p-value (p = 5.6×10−8). NOX significantly associated with cg11756214 within ZNF347 (p = 5.6×10−8). Several differentially methylated signals were also associated with cis-gene expression. The DMR located on chromosome 7 was associated with the expression of HOXA5, HOXA9, and HOXA10. The DMRs located on chromosomes 5 and 16 were associated with expression of MRPL36 and DEXI, respectively. The CpG cg05926640 was associated with expression of ARID4B, IRF2BP2, and TOMM20. We identified differential DNA methylation in monocytes associated with long-term air pollution exposure. Methylation signals associated with gene expression might help explain how air pollution contributes to cardiovascular disease. Air pollution might affect atherosclerosis through DNA methylation changes in cells crucial to atherosclerosis, such as monocytes. We conducted an epigenome-wide study of DNA methylation in CD14+ monocytes and long-term ambient air pollution exposure in adults participating in the Multi-Ethnic Study of Atherosclerosis (MESA). We also assessed the association between differentially methylated signals and -gene expression. Using spatiotemporal models, one-year average concentrations of outdoor fine particulate matter (PM ) and oxides of nitrogen (NO ) were estimated at participants' homes. We assessed DNA methylation and gene expression using Illumina 450k and HumanHT-12 v4 Expression BeadChips, respectively (n = 1,207). We used bump hunting and site-specific approaches to identify differentially methylated signals (false discovery rate of 0.05) and used linear models to assess associations between differentially methylated signals and -gene expression. Four differentially methylated regions (DMRs) located on chromosomes 5, 6, 7, and 16 (within or near , and , respectively) were associated with PM . The DMRs on chromosomes 5 and 6 also associated with NO . The DMR on chromosome 5 had the smallest p-value for both PM (p = 1.4×10 ) and NO (p = 7.7×10 ). Three differentially methylated CpGs were identified for PM , and cg05926640 (near ) had the smallest p-value (p = 5.6×10 ). NO significantly associated with cg11756214 within (p = 5.6×10 ). Several differentially methylated signals were also associated with -gene expression. The DMR located on chromosome 7 was associated with the expression of , and . The DMRs located on chromosomes 5 and 16 were associated with expression of and , respectively. The CpG cg05926640 was associated with expression of , and . We identified differential DNA methylation in monocytes associated with long-term air pollution exposure. Methylation signals associated with gene expression might help explain how air pollution contributes to cardiovascular disease. |
| Author | Liu, Yongmei Enquobahrie, Daniel A. Reynolds, Lindsay M. Lee, Su-In Chi, Gloria C. Siscovick, David MacDonald, James W. Fitzpatrick, Annette L. Budoff, Matthew J. Kaufman, Joel D. Kerr, Kathleen F. |
| Author_xml | – sequence: 1 givenname: Gloria C. surname: Chi fullname: Chi, Gloria C. email: glochi@uw.edu organization: University of Washington – sequence: 2 givenname: Yongmei surname: Liu fullname: Liu, Yongmei organization: Wake Forest School of Medicine – sequence: 3 givenname: James W. orcidid: 0000-0002-7328-7626 surname: MacDonald fullname: MacDonald, James W. organization: University of Washington – sequence: 4 givenname: Lindsay M. surname: Reynolds fullname: Reynolds, Lindsay M. organization: Wake Forest School of Medicine – sequence: 5 givenname: Daniel A. surname: Enquobahrie fullname: Enquobahrie, Daniel A. organization: University of Washington – sequence: 6 givenname: Annette L. surname: Fitzpatrick fullname: Fitzpatrick, Annette L. organization: University of Washington – sequence: 7 givenname: Kathleen F. surname: Kerr fullname: Kerr, Kathleen F. organization: University of Washington – sequence: 8 givenname: Matthew J. surname: Budoff fullname: Budoff, Matthew J. organization: Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center – sequence: 9 givenname: Su-In surname: Lee fullname: Lee, Su-In organization: University of Washington – sequence: 10 givenname: David surname: Siscovick fullname: Siscovick, David organization: New York Academy of Medicine – sequence: 11 givenname: Joel D. surname: Kaufman fullname: Kaufman, Joel D. organization: University of Washington |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33818294$$D View this record in MEDLINE/PubMed |
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| Snippet | Air pollution might affect atherosclerosis through DNA methylation changes in cells crucial to atherosclerosis, such as monocytes. We conducted an... |
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| SubjectTerms | Adult Air Pollutants - toxicity Air pollution Air Pollution - analysis Air Pollution - statistics & numerical data Antigens, Neoplasm - analysis Atherosclerosis - chemically induced Atherosclerosis - genetics DNA Methylation Environmental Exposure - analysis Environmental Exposure - statistics & numerical data Epigenome fine particulate matter gene expression Humans Monocytes Neoplasm Proteins oxides of nitrogen Particulate Matter - toxicity Research Paper |
| Title | Epigenome-wide analysis of long-term air pollution exposure and DNA methylation in monocytes: results from the Multi-Ethnic Study of Atherosclerosis |
| URI | https://www.tandfonline.com/doi/abs/10.1080/15592294.2021.1900028 https://www.ncbi.nlm.nih.gov/pubmed/33818294 https://www.proquest.com/docview/2508892135 https://pubmed.ncbi.nlm.nih.gov/PMC8920186 https://doaj.org/article/1600c9174ceb405ea5453c6ea155a636 |
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