Mitochondrial Gene Expression Profiles Are Associated with Maternal Psychosocial Stress in Pregnancy and Infant Temperament
Gene-environment interactions mediate through the placenta and shape the fetal brain development. Between the environmental determinants of the fetal brain, maternal psychosocial stress in pregnancy has been shown to negatively influence the infant temperament development. This in turn may have adve...
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| description | Gene-environment interactions mediate through the placenta and shape the fetal brain development. Between the environmental determinants of the fetal brain, maternal psychosocial stress in pregnancy has been shown to negatively influence the infant temperament development. This in turn may have adverse consequences on the infant neurodevelopment extending throughout the entire life-span. However little is known about the underlying biological mechanisms of the effects of maternal psychosocial stress in pregnancy on infant temperament. Environmental stressors such as maternal psychosocial stress in pregnancy activate the stress response cascade that in turn drives the increase in the cellular energy demand of vital organs with high metabolic rates such as, in pregnancy, the placenta. Key players of the stress response cascade are the mitochondria.
Here, we tested the expression of all 13 protein-coding genes encoded by the mitochondria in 108 placenta samples from the Stress in Pregnancy birth cohort, a study that aims at determining the influence of in utero exposure to maternal psychosocial stress in pregnancy on infant temperament. We showed that the expression of the protein-coding mitochondrial-encoded gene MT-ND2 was positively associated with indices of maternal psychosocial stress in pregnancy including Prenatal Perceived Stress (β = 0.259; p-regression = 0.004; r2-regression = 0.120), State Anxiety (β = 0.218; p-regression = 0.003; r2-regression = 0.153), Trait Anxiety (β = 0.262; p-regression = 0.003; r2-regression = 0.129) and Pregnancy Anxiety Total (β = 0.208; p-regression = 0.010; r2-regression = 0.103). In the meantime MT-ND2 was negatively associated with the infant temperament indices of Activity Level (β = -0.257; p-regression = 0.008; r2-regression = 0.165) and Smile and Laughter (β = -0.286; p-regression = 0.036; r2-regression = 0.082). Additionally, MT-ND6 was associated with the maternal psychosocial stress in pregnancy index of Prenatal Perceived Stress (β = -0.231; p-regression = 0.004; r2-regression = 0.120), while MT-CO2 was associated with the maternal psychosocial stress in pregnancy indices of State Anxiety (β = 0.206; p-regression = 0.003; r2-regression = 0.153) and Trait Anxiety (β = 0.205; p-regression = 0.003; r2-regression = 0.129).
Our data support the role of mitochondria in responding to maternal psychosocial stress in pregnancy, as assessed in placenta, while also suggesting an important role for the mitochondria in the |
| doi_str_mv | 10.1371/journal.pone.0138929 |
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Here, we tested the expression of all 13 protein-coding genes encoded by the mitochondria in 108 placenta samples from the Stress in Pregnancy birth cohort, a study that aims at determining the influence of in utero exposure to maternal psychosocial stress in pregnancy on infant temperament. We showed that the expression of the protein-coding mitochondrial-encoded gene MT-ND2 was positively associated with indices of maternal psychosocial stress in pregnancy including Prenatal Perceived Stress (β = 0.259; p-regression = 0.004; r2-regression = 0.120), State Anxiety (β = 0.218; p-regression = 0.003; r2-regression = 0.153), Trait Anxiety (β = 0.262; p-regression = 0.003; r2-regression = 0.129) and Pregnancy Anxiety Total (β = 0.208; p-regression = 0.010; r2-regression = 0.103). In the meantime MT-ND2 was negatively associated with the infant temperament indices of Activity Level (β = -0.257; p-regression = 0.008; r2-regression = 0.165) and Smile and Laughter (β = -0.286; p-regression = 0.036; r2-regression = 0.082). Additionally, MT-ND6 was associated with the maternal psychosocial stress in pregnancy index of Prenatal Perceived Stress (β = -0.231; p-regression = 0.004; r2-regression = 0.120), while MT-CO2 was associated with the maternal psychosocial stress in pregnancy indices of State Anxiety (β = 0.206; p-regression = 0.003; r2-regression = 0.153) and Trait Anxiety (β = 0.205; p-regression = 0.003; r2-regression = 0.129).
Our data support the role of mitochondria in responding to maternal psychosocial stress in pregnancy, as assessed in placenta, while also suggesting an important role for the mitochondria in the infant temperament development.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0138929</identifier><identifier>PMID: 26418562</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Anxiety ; Biological effects ; Biology ; Brain ; Carbon dioxide ; Cellular stress response ; Child & adolescent psychiatry ; Coding ; Cohort Studies ; Energy demand ; Environmental stress ; Female ; Fetal Development ; Fetuses ; Gene expression ; Genes, Mitochondrial - genetics ; Genetic aspects ; Genotype-environment interactions ; Glucose ; Homeostasis ; Humans ; Infant ; Infant Behavior - physiology ; Infants ; Intrauterine exposure ; Male ; Metabolism ; Mitochondria ; Mitochondrial DNA ; Neural coding ; Neurodevelopment ; Organs ; Parents & parenting ; Phosphorylation ; Physiological aspects ; Physiology ; Placenta ; Placenta - metabolism ; Pregnancy ; Pregnancy Complications - genetics ; Pregnancy Complications - psychology ; Pregnant women ; Prenatal experience ; Preventive medicine ; Proteins ; Psychological aspects ; Psychopathology ; Questionnaires ; Regression ; Social interactions ; Stress ; Stress (Psychology) ; Stress response ; Stress, Psychological - genetics ; Stresses ; Temperament - physiology ; Transcriptome</subject><ispartof>PloS one, 2015-09, Vol.10 (9), p.e0138929-e0138929</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Lambertini et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Lambertini et al 2015 Lambertini et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-3d2b95b215bab7cdb0cb7c282013791c2fd1cba7af993bbcf9b55fa09b22d0e43</citedby><cites>FETCH-LOGICAL-c692t-3d2b95b215bab7cdb0cb7c282013791c2fd1cba7af993bbcf9b55fa09b22d0e43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4587925/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4587925/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26418562$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Cordero, Mario D.</contributor><creatorcontrib>Lambertini, Luca</creatorcontrib><creatorcontrib>Chen, Jia</creatorcontrib><creatorcontrib>Nomura, Yoko</creatorcontrib><title>Mitochondrial Gene Expression Profiles Are Associated with Maternal Psychosocial Stress in Pregnancy and Infant Temperament</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Gene-environment interactions mediate through the placenta and shape the fetal brain development. Between the environmental determinants of the fetal brain, maternal psychosocial stress in pregnancy has been shown to negatively influence the infant temperament development. This in turn may have adverse consequences on the infant neurodevelopment extending throughout the entire life-span. However little is known about the underlying biological mechanisms of the effects of maternal psychosocial stress in pregnancy on infant temperament. Environmental stressors such as maternal psychosocial stress in pregnancy activate the stress response cascade that in turn drives the increase in the cellular energy demand of vital organs with high metabolic rates such as, in pregnancy, the placenta. Key players of the stress response cascade are the mitochondria.
Here, we tested the expression of all 13 protein-coding genes encoded by the mitochondria in 108 placenta samples from the Stress in Pregnancy birth cohort, a study that aims at determining the influence of in utero exposure to maternal psychosocial stress in pregnancy on infant temperament. We showed that the expression of the protein-coding mitochondrial-encoded gene MT-ND2 was positively associated with indices of maternal psychosocial stress in pregnancy including Prenatal Perceived Stress (β = 0.259; p-regression = 0.004; r2-regression = 0.120), State Anxiety (β = 0.218; p-regression = 0.003; r2-regression = 0.153), Trait Anxiety (β = 0.262; p-regression = 0.003; r2-regression = 0.129) and Pregnancy Anxiety Total (β = 0.208; p-regression = 0.010; r2-regression = 0.103). In the meantime MT-ND2 was negatively associated with the infant temperament indices of Activity Level (β = -0.257; p-regression = 0.008; r2-regression = 0.165) and Smile and Laughter (β = -0.286; p-regression = 0.036; r2-regression = 0.082). Additionally, MT-ND6 was associated with the maternal psychosocial stress in pregnancy index of Prenatal Perceived Stress (β = -0.231; p-regression = 0.004; r2-regression = 0.120), while MT-CO2 was associated with the maternal psychosocial stress in pregnancy indices of State Anxiety (β = 0.206; p-regression = 0.003; r2-regression = 0.153) and Trait Anxiety (β = 0.205; p-regression = 0.003; r2-regression = 0.129).
Our data support the role of mitochondria in responding to maternal psychosocial stress in pregnancy, as assessed in placenta, while also suggesting an important role for the mitochondria in the infant temperament development.</description><subject>Adult</subject><subject>Anxiety</subject><subject>Biological effects</subject><subject>Biology</subject><subject>Brain</subject><subject>Carbon dioxide</subject><subject>Cellular stress response</subject><subject>Child & adolescent psychiatry</subject><subject>Coding</subject><subject>Cohort Studies</subject><subject>Energy demand</subject><subject>Environmental stress</subject><subject>Female</subject><subject>Fetal Development</subject><subject>Fetuses</subject><subject>Gene expression</subject><subject>Genes, Mitochondrial - genetics</subject><subject>Genetic aspects</subject><subject>Genotype-environment interactions</subject><subject>Glucose</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Infant</subject><subject>Infant Behavior - physiology</subject><subject>Infants</subject><subject>Intrauterine exposure</subject><subject>Male</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Mitochondrial DNA</subject><subject>Neural coding</subject><subject>Neurodevelopment</subject><subject>Organs</subject><subject>Parents & parenting</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Physiology</subject><subject>Placenta</subject><subject>Placenta - metabolism</subject><subject>Pregnancy</subject><subject>Pregnancy Complications - genetics</subject><subject>Pregnancy Complications - psychology</subject><subject>Pregnant women</subject><subject>Prenatal experience</subject><subject>Preventive medicine</subject><subject>Proteins</subject><subject>Psychological aspects</subject><subject>Psychopathology</subject><subject>Questionnaires</subject><subject>Regression</subject><subject>Social interactions</subject><subject>Stress</subject><subject>Stress (Psychology)</subject><subject>Stress response</subject><subject>Stress, Psychological - 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genetics</topic><topic>Genetic aspects</topic><topic>Genotype-environment interactions</topic><topic>Glucose</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Infant</topic><topic>Infant Behavior - physiology</topic><topic>Infants</topic><topic>Intrauterine exposure</topic><topic>Male</topic><topic>Metabolism</topic><topic>Mitochondria</topic><topic>Mitochondrial DNA</topic><topic>Neural coding</topic><topic>Neurodevelopment</topic><topic>Organs</topic><topic>Parents & parenting</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>Physiology</topic><topic>Placenta</topic><topic>Placenta - metabolism</topic><topic>Pregnancy</topic><topic>Pregnancy Complications - genetics</topic><topic>Pregnancy Complications - psychology</topic><topic>Pregnant women</topic><topic>Prenatal experience</topic><topic>Preventive medicine</topic><topic>Proteins</topic><topic>Psychological aspects</topic><topic>Psychopathology</topic><topic>Questionnaires</topic><topic>Regression</topic><topic>Social interactions</topic><topic>Stress</topic><topic>Stress (Psychology)</topic><topic>Stress response</topic><topic>Stress, Psychological - genetics</topic><topic>Stresses</topic><topic>Temperament - physiology</topic><topic>Transcriptome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lambertini, Luca</creatorcontrib><creatorcontrib>Chen, Jia</creatorcontrib><creatorcontrib>Nomura, Yoko</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lambertini, Luca</au><au>Chen, Jia</au><au>Nomura, Yoko</au><au>Cordero, Mario D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitochondrial Gene Expression Profiles Are Associated with Maternal Psychosocial Stress in Pregnancy and Infant Temperament</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-09-29</date><risdate>2015</risdate><volume>10</volume><issue>9</issue><spage>e0138929</spage><epage>e0138929</epage><pages>e0138929-e0138929</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Gene-environment interactions mediate through the placenta and shape the fetal brain development. Between the environmental determinants of the fetal brain, maternal psychosocial stress in pregnancy has been shown to negatively influence the infant temperament development. This in turn may have adverse consequences on the infant neurodevelopment extending throughout the entire life-span. However little is known about the underlying biological mechanisms of the effects of maternal psychosocial stress in pregnancy on infant temperament. Environmental stressors such as maternal psychosocial stress in pregnancy activate the stress response cascade that in turn drives the increase in the cellular energy demand of vital organs with high metabolic rates such as, in pregnancy, the placenta. Key players of the stress response cascade are the mitochondria.
Here, we tested the expression of all 13 protein-coding genes encoded by the mitochondria in 108 placenta samples from the Stress in Pregnancy birth cohort, a study that aims at determining the influence of in utero exposure to maternal psychosocial stress in pregnancy on infant temperament. We showed that the expression of the protein-coding mitochondrial-encoded gene MT-ND2 was positively associated with indices of maternal psychosocial stress in pregnancy including Prenatal Perceived Stress (β = 0.259; p-regression = 0.004; r2-regression = 0.120), State Anxiety (β = 0.218; p-regression = 0.003; r2-regression = 0.153), Trait Anxiety (β = 0.262; p-regression = 0.003; r2-regression = 0.129) and Pregnancy Anxiety Total (β = 0.208; p-regression = 0.010; r2-regression = 0.103). In the meantime MT-ND2 was negatively associated with the infant temperament indices of Activity Level (β = -0.257; p-regression = 0.008; r2-regression = 0.165) and Smile and Laughter (β = -0.286; p-regression = 0.036; r2-regression = 0.082). Additionally, MT-ND6 was associated with the maternal psychosocial stress in pregnancy index of Prenatal Perceived Stress (β = -0.231; p-regression = 0.004; r2-regression = 0.120), while MT-CO2 was associated with the maternal psychosocial stress in pregnancy indices of State Anxiety (β = 0.206; p-regression = 0.003; r2-regression = 0.153) and Trait Anxiety (β = 0.205; p-regression = 0.003; r2-regression = 0.129).
Our data support the role of mitochondria in responding to maternal psychosocial stress in pregnancy, as assessed in placenta, while also suggesting an important role for the mitochondria in the infant temperament development.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26418562</pmid><doi>10.1371/journal.pone.0138929</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2015-09, Vol.10 (9), p.e0138929-e0138929 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1719322336 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adult Anxiety Biological effects Biology Brain Carbon dioxide Cellular stress response Child & adolescent psychiatry Coding Cohort Studies Energy demand Environmental stress Female Fetal Development Fetuses Gene expression Genes, Mitochondrial - genetics Genetic aspects Genotype-environment interactions Glucose Homeostasis Humans Infant Infant Behavior - physiology Infants Intrauterine exposure Male Metabolism Mitochondria Mitochondrial DNA Neural coding Neurodevelopment Organs Parents & parenting Phosphorylation Physiological aspects Physiology Placenta Placenta - metabolism Pregnancy Pregnancy Complications - genetics Pregnancy Complications - psychology Pregnant women Prenatal experience Preventive medicine Proteins Psychological aspects Psychopathology Questionnaires Regression Social interactions Stress Stress (Psychology) Stress response Stress, Psychological - genetics Stresses Temperament - physiology Transcriptome |
| title | Mitochondrial Gene Expression Profiles Are Associated with Maternal Psychosocial Stress in Pregnancy and Infant Temperament |
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