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Maternal factors are associated with the expression of placental genes involved in amino acid metabolism and transport

Maternal factors are associated with the expression of placental genes involved in amino acid metabolism and transport
Maternal factors are associated with the expression of placental genes involved in amino acid metabolism and transport
NTRODUCTION: Maternal environment and lifestyle factors may modify placental function to match the mother's capacity to support the demands of fetal growth. Much remains to be understood about maternal influences on placental metabolic and amino acid transporter gene expression. We investigated the influences of maternal lifestyle and body composition (e.g. fat and muscle content) on a selection of metabolic and amino acid transporter genes and their associations with fetal growth.

METHODS: RNA was extracted from 102 term Southampton Women's Survey placental samples. Expression of nine metabolic, seven exchange, eight accumulative and three facilitated transporter genes was analyzed using quantitative real-time PCR.

RESULTS: Increased placental LAT2 (p = 0.01), y+LAT2 (p = 0.03), aspartate aminotransferase 2 (p = 0.02) and decreased aspartate aminotransferase 1 (p = 0.04) mRNA expression associated with pre-pregnancy maternal smoking. Placental mRNA expression of TAT1 (p = 0.01), ASCT1 (p = 0.03), mitochondrial branched chain aminotransferase (p = 0.02) and glutamine synthetase (p = 0.05) was positively associated with maternal strenuous exercise. Increased glutamine synthetase mRNA expression (r = 0.20, p = 0.05) associated with higher maternal diet quality (prudent dietary pattern) pre-pregnancy. Lower LAT4 (r = -0.25, p = 0.05) and aspartate aminotransferase 2 mRNA expression (r = -0.28, p = 0.01) associated with higher early pregnancy diet quality. Lower placental ASCT1 mRNA expression associated with measures of increased maternal fat mass, including pre-pregnancy BMI (r = -0.26, p = 0.01). Lower placental mRNA expression of alanine aminotransferase 2 associated with greater neonatal adiposity, for example neonatal subscapular skinfold thickness (r = -0.33, p = 0.001).

CONCLUSION: A number of maternal influences have been linked with outcomes in childhood, independently of neonatal size; our finding of associations between placental expression of transporter and metabolic genes and maternal smoking, physical activity and diet raises the possibility that their effects are mediated in part through alterations in placental function. The observed changes in placental gene expression in relation to modifiable maternal factors are important as they could form part of interventions aimed at maintaining a healthy lifestyle for the mother and for optimal fetal development.
1932-6203
1-17
Day, P.E.
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Ntani, G.
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Crozier, S.R.
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Mahon, P.A.
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Inskip, H.M.
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Cooper, C.
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Harvey, N.C.
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Godfrey, K.M.
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Hanson, M.A.
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Lewis, R.M.
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Cleal, J.K.
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Day, P.E.
368665e9-66a3-45ee-94b3-ef130f37af69
Ntani, G.
9b009e0a-5ab2-4c6e-a9fd-15a601e92be5
Crozier, S.R.
9c3595ce-45b0-44fa-8c4c-4c555e628a03
Mahon, P.A.
5a824126-9030-4e8a-9a0e-dafb8aa280f9
Inskip, H.M.
5fb4470a-9379-49b2-a533-9da8e61058b7
Cooper, C.
e05f5612-b493-4273-9b71-9e0ce32bdad6
Harvey, N.C.
ce487fb4-d360-4aac-9d17-9466d6cba145
Godfrey, K.M.
0931701e-fe2c-44b5-8f0d-ec5c7477a6fd
Hanson, M.A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Lewis, R.M.
caaeb97d-ea69-4f7b-8adb-5fa25e2d3502
Cleal, J.K.
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Day, P.E., Ntani, G., Crozier, S.R., Mahon, P.A., Inskip, H.M., Cooper, C., Harvey, N.C., Godfrey, K.M., Hanson, M.A., Lewis, R.M. and Cleal, J.K. (2015) Maternal factors are associated with the expression of placental genes involved in amino acid metabolism and transport. PLoS ONE, 10 (12), 1-17, [e0143653]. (doi:10.1371/journal.pone.0143653). (PMID:26657885)

Record type: Article

Abstract

NTRODUCTION: Maternal environment and lifestyle factors may modify placental function to match the mother's capacity to support the demands of fetal growth. Much remains to be understood about maternal influences on placental metabolic and amino acid transporter gene expression. We investigated the influences of maternal lifestyle and body composition (e.g. fat and muscle content) on a selection of metabolic and amino acid transporter genes and their associations with fetal growth.

METHODS: RNA was extracted from 102 term Southampton Women's Survey placental samples. Expression of nine metabolic, seven exchange, eight accumulative and three facilitated transporter genes was analyzed using quantitative real-time PCR.

RESULTS: Increased placental LAT2 (p = 0.01), y+LAT2 (p = 0.03), aspartate aminotransferase 2 (p = 0.02) and decreased aspartate aminotransferase 1 (p = 0.04) mRNA expression associated with pre-pregnancy maternal smoking. Placental mRNA expression of TAT1 (p = 0.01), ASCT1 (p = 0.03), mitochondrial branched chain aminotransferase (p = 0.02) and glutamine synthetase (p = 0.05) was positively associated with maternal strenuous exercise. Increased glutamine synthetase mRNA expression (r = 0.20, p = 0.05) associated with higher maternal diet quality (prudent dietary pattern) pre-pregnancy. Lower LAT4 (r = -0.25, p = 0.05) and aspartate aminotransferase 2 mRNA expression (r = -0.28, p = 0.01) associated with higher early pregnancy diet quality. Lower placental ASCT1 mRNA expression associated with measures of increased maternal fat mass, including pre-pregnancy BMI (r = -0.26, p = 0.01). Lower placental mRNA expression of alanine aminotransferase 2 associated with greater neonatal adiposity, for example neonatal subscapular skinfold thickness (r = -0.33, p = 0.001).

CONCLUSION: A number of maternal influences have been linked with outcomes in childhood, independently of neonatal size; our finding of associations between placental expression of transporter and metabolic genes and maternal smoking, physical activity and diet raises the possibility that their effects are mediated in part through alterations in placental function. The observed changes in placental gene expression in relation to modifiable maternal factors are important as they could form part of interventions aimed at maintaining a healthy lifestyle for the mother and for optimal fetal development.

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More information

Accepted/In Press date: 7 November 2015
e-pub ahead of print date: 14 December 2015
Published date: 14 December 2015
Organisations: Faculty of Medicine

Identifiers

Local EPrints ID: 385143
URI: http://eprints.soton.ac.uk/id/eprint/385143
ISSN: 1932-6203
PURE UUID: c0aa087c-68e8-444a-b9f0-0f1393fbcbe7
ORCID for S.R. Crozier: ORCID iD orcid.org/0000-0002-9524-1127
ORCID for H.M. Inskip: ORCID iD orcid.org/0000-0001-8897-1749
ORCID for C. Cooper: ORCID iD orcid.org/0000-0003-3510-0709
ORCID for N.C. Harvey: ORCID iD orcid.org/0000-0002-8194-2512
ORCID for K.M. Godfrey: ORCID iD orcid.org/0000-0002-4643-0618
ORCID for M.A. Hanson: ORCID iD orcid.org/0000-0002-6907-613X
ORCID for R.M. Lewis: ORCID iD orcid.org/0000-0003-4044-9104
ORCID for J.K. Cleal: ORCID iD orcid.org/0000-0001-7978-4327

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Date deposited: 15 Jan 2016 15:35
Last modified: 18 Feb 2021 17:02

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