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Perinatal DNA methylation at CDKN2A is associated with offspring bone mass: findings from the Southampton Women's Survey

Perinatal DNA methylation at CDKN2A is associated with offspring bone mass: findings from the Southampton Women's Survey
Perinatal DNA methylation at CDKN2A is associated with offspring bone mass: findings from the Southampton Women's Survey
Poor intrauterine and childhood growth has been linked with the risk of osteoporosis in later life, a relationship which may in part be mediated through altered epigenetic regulation of genes. We previously identified a region within the promoter of the long non-coding RNA ANRIL encoded by the CDKN2A locus, at which differential DNA methylation at birth showed correlations with offspring adiposity. Given the common lineage of adipocytes and osteoblasts, we investigated the relationship between perinatal CDKN2A methylation and bone mass at ages 4 and 6 years. Using sodium bisulfite pyrosequencing we measured the methylation status of the 9 CpGs within this region in umbilical cord samples from discovery (n = 332) and replication (n = 337) cohorts of children from the Southampton Women's Survey, whose bone mass was assessed by DXA (Hologic Discovery). Inverse associations were found between perinatal CDKN2A methylation and whole body minus head bone area (BA), bone mineral content (BMC) and areal bone-mineral density (BMD). This was confirmed in replication and combined data sets (all p < 0.01), with each 10% increase in methylation being associated with a decrease in BMC of 4-9 g at age 4 years (p≤0.001). Relationships were similar with 6 year bone mass. Functional investigation of the differentially methylated region in the SaOS-2 osteosarcoma cell line showed that transcription factors bound to the identified CpGs in a methylation specific manner, and that CpG mutagenesis modulated ANRIL expression. In conclusion, perinatal methylation at CDKN2A is associated with childhood bone development, and has significance for cell function.
0884-0431
2030-2040
Curtis, Elizabeth M.
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Murray, Robert
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Titcombe, Philip
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Cook, Eloise
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Clarke-Harris, Rebecca
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Costello, Paula
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Garratt, Emma
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Holbrook, Joanna D.
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Barton, Sheila
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Inskip, Hazel
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Godfrey, Keith M.
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Bell, Christopher G.
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Cooper, Cyrus
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Lillycrop, Karen A.
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Harvey, Nicholas C.
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Curtis, Elizabeth M.
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Murray, Robert
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Titcombe, Philip
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Cook, Eloise
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Clarke-Harris, Rebecca
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Costello, Paula
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Garratt, Emma
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Holbrook, Joanna D.
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Barton, Sheila
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Inskip, Hazel
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Godfrey, Keith M.
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Bell, Christopher G.
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Cooper, Cyrus
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Lillycrop, Karen A.
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Harvey, Nicholas C.
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Curtis, Elizabeth M., Murray, Robert, Titcombe, Philip, Cook, Eloise, Clarke-Harris, Rebecca, Costello, Paula, Garratt, Emma, Holbrook, Joanna D., Barton, Sheila, Inskip, Hazel, Godfrey, Keith M., Bell, Christopher G., Cooper, Cyrus, Lillycrop, Karen A. and Harvey, Nicholas C. (2017) Perinatal DNA methylation at CDKN2A is associated with offspring bone mass: findings from the Southampton Women's Survey. Journal of Bone and Mineral Research, 32 (10), 2030-2040. (doi:10.1002/jbmr.3153).

Record type: Article

Abstract

Poor intrauterine and childhood growth has been linked with the risk of osteoporosis in later life, a relationship which may in part be mediated through altered epigenetic regulation of genes. We previously identified a region within the promoter of the long non-coding RNA ANRIL encoded by the CDKN2A locus, at which differential DNA methylation at birth showed correlations with offspring adiposity. Given the common lineage of adipocytes and osteoblasts, we investigated the relationship between perinatal CDKN2A methylation and bone mass at ages 4 and 6 years. Using sodium bisulfite pyrosequencing we measured the methylation status of the 9 CpGs within this region in umbilical cord samples from discovery (n = 332) and replication (n = 337) cohorts of children from the Southampton Women's Survey, whose bone mass was assessed by DXA (Hologic Discovery). Inverse associations were found between perinatal CDKN2A methylation and whole body minus head bone area (BA), bone mineral content (BMC) and areal bone-mineral density (BMD). This was confirmed in replication and combined data sets (all p < 0.01), with each 10% increase in methylation being associated with a decrease in BMC of 4-9 g at age 4 years (p≤0.001). Relationships were similar with 6 year bone mass. Functional investigation of the differentially methylated region in the SaOS-2 osteosarcoma cell line showed that transcription factors bound to the identified CpGs in a methylation specific manner, and that CpG mutagenesis modulated ANRIL expression. In conclusion, perinatal methylation at CDKN2A is associated with childhood bone development, and has significance for cell function.

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CDKN2A bone paper 28_02_2017 nch - Accepted Manuscript
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Accepted/In Press date: 7 April 2017
e-pub ahead of print date: 17 April 2017
Published date: October 2017
Organisations: Epidemiology, Medical Research Council, Human Development & Health, Epigenetics, Centre for Biological Sciences

Identifiers

Local EPrints ID: 407851
URI: http://eprints.soton.ac.uk/id/eprint/407851
ISSN: 0884-0431
PURE UUID: 5b19cee8-186b-42f8-8a2b-82687dfde596
ORCID for Elizabeth M. Curtis: ORCID iD orcid.org/0000-0002-5147-0550
ORCID for Philip Titcombe: ORCID iD orcid.org/0000-0002-7797-8571
ORCID for Rebecca Clarke-Harris: ORCID iD orcid.org/0000-0002-6888-9518
ORCID for Emma Garratt: ORCID iD orcid.org/0000-0001-5268-4203
ORCID for Joanna D. Holbrook: ORCID iD orcid.org/0000-0003-1791-6894
ORCID for Sheila Barton: ORCID iD orcid.org/0000-0003-4963-4242
ORCID for Hazel Inskip: ORCID iD orcid.org/0000-0001-8897-1749
ORCID for Keith M. Godfrey: ORCID iD orcid.org/0000-0002-4643-0618
ORCID for Christopher G. Bell: ORCID iD orcid.org/0000-0003-4601-1242
ORCID for Cyrus Cooper: ORCID iD orcid.org/0000-0003-3510-0709
ORCID for Karen A. Lillycrop: ORCID iD orcid.org/0000-0001-7350-5489
ORCID for Nicholas C. Harvey: ORCID iD orcid.org/0000-0002-8194-2512

Catalogue record

Date deposited: 27 Apr 2017 01:05
Last modified: 18 Mar 2024 05:12

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Contributors

Author: Robert Murray
Author: Philip Titcombe ORCID iD
Author: Eloise Cook
Author: Rebecca Clarke-Harris ORCID iD
Author: Paula Costello
Author: Emma Garratt ORCID iD
Author: Joanna D. Holbrook ORCID iD
Author: Sheila Barton ORCID iD
Author: Hazel Inskip ORCID iD
Author: Christopher G. Bell ORCID iD
Author: Cyrus Cooper ORCID iD

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