The cardiovascular and hypothalamus-pituitary-adrenal axis response to stress is controlled by glucocorticoid receptor sequence variants and promoter methylation.
Identifieur interne : 000074 ( PubMed/Checkpoint ); précédent : 000073; suivant : 000075The cardiovascular and hypothalamus-pituitary-adrenal axis response to stress is controlled by glucocorticoid receptor sequence variants and promoter methylation.
Auteurs : Ting Li-Tempel [Allemagne] ; Mauro F. Larra [Allemagne] ; Estelle Sandt [Luxembourg (pays)] ; Sophie B. Mériaux [Luxembourg (pays)] ; Andrea B. Schote [Allemagne] ; Hartmut Sch Chinger [Allemagne] ; Claude P. Muller [Allemagne] ; Jonathan D. Turner [Luxembourg (pays)]Source :
- Clinical epigenetics [ 1868-7075 ] ; 2016.
English descriptors
- KwdEn :
- Blood Pressure (genetics), Blood Pressure (physiology), DNA Methylation, Female, Genetic Variation (genetics), Genetic Variation (physiology), Genotype, Haplotypes (genetics), Humans, Hydrocortisone (analysis), Hydrocortisone (physiology), Male, Promoter Regions, Genetic (genetics), Receptors, Glucocorticoid (genetics), Receptors, Glucocorticoid (physiology), Saliva (chemistry), Stress, Psychological (genetics), Stress, Psychological (physiopathology), Young Adult.
- MESH :
- chemical , analysis : Hydrocortisone.
- chemistry : Saliva.
- genetics : Blood Pressure, Genetic Variation, Haplotypes, Promoter Regions, Genetic, Receptors, Glucocorticoid, Stress, Psychological.
- physiology : Blood Pressure, Genetic Variation, Hydrocortisone, Receptors, Glucocorticoid.
- physiopathology : Stress, Psychological.
- DNA Methylation, Female, Genotype, Humans, Male, Young Adult.
Abstract
Gender, genetic makeup, and prior experience interact to determine physiological responses to an external perceived stressor. Here, we investigated the contribution of both genetic variants and promoter methylation of the NR3C1 (glucocorticoid receptor) gene to the cardiovascular and hypothalamus-pituitary-adrenal (HPA) axis response to the socially evaluated cold pressor test (seCPT).
DOI: 10.1186/s13148-016-0180-y
PubMed: 26823689
Affiliations:
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Larra</name><affiliation wicri:level="4"><nlm:affiliation>Department of Clinical Physiology, Research Institute of Psychobiology, University of Trier, 54290 Trier, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Clinical Physiology, Research Institute of Psychobiology, University of Trier, 54290 Trier</wicri:regionArea><wicri:noRegion>54290 Trier</wicri:noRegion><orgName type="university">Université de Trèves</orgName><placeName><settlement type="city">Trèves (Allemagne)</settlement><region type="land" nuts="1">Rhénanie-Palatinat</region></placeName></affiliation></author><author><name sortKey="Sandt, Estelle" sort="Sandt, Estelle" uniqKey="Sandt E" first="Estelle" last="Sandt">Estelle Sandt</name><affiliation wicri:level="1"><nlm:affiliation>Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, Esch-sur-Alzette, 4354 Grand-Duchy of Luxembourg.</nlm:affiliation><country xml:lang="fr">Luxembourg (pays)</country><wicri:regionArea>Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, Esch-sur-Alzette</wicri:regionArea><wicri:noRegion>Esch-sur-Alzette</wicri:noRegion></affiliation></author><author><name sortKey="Meriaux, Sophie B" sort="Meriaux, Sophie B" uniqKey="Meriaux S" first="Sophie B" last="Mériaux">Sophie B. Mériaux</name><affiliation wicri:level="1"><nlm:affiliation>Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, Esch-sur-Alzette, 4354 Grand-Duchy of Luxembourg.</nlm:affiliation><country xml:lang="fr">Luxembourg (pays)</country><wicri:regionArea>Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, Esch-sur-Alzette</wicri:regionArea><wicri:noRegion>Esch-sur-Alzette</wicri:noRegion></affiliation></author><author><name sortKey="Schote, Andrea B" sort="Schote, Andrea B" uniqKey="Schote A" first="Andrea B" last="Schote">Andrea B. Schote</name><affiliation wicri:level="4"><nlm:affiliation>Department of Neurobehavioral Genetics, Research Institute of Psychobiology, University of Trier, 54290 Trier, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurobehavioral Genetics, Research Institute of Psychobiology, University of Trier, 54290 Trier</wicri:regionArea><wicri:noRegion>54290 Trier</wicri:noRegion><orgName type="university">Université de Trèves</orgName><placeName><settlement type="city">Trèves (Allemagne)</settlement><region type="land" nuts="1">Rhénanie-Palatinat</region></placeName></affiliation></author><author><name sortKey="Sch Chinger, Hartmut" sort="Sch Chinger, Hartmut" uniqKey="Sch Chinger H" first="Hartmut" last="Sch Chinger">Hartmut Sch Chinger</name><affiliation wicri:level="4"><nlm:affiliation>Department of Clinical Physiology, Research Institute of Psychobiology, University of Trier, 54290 Trier, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Clinical Physiology, Research Institute of Psychobiology, University of Trier, 54290 Trier</wicri:regionArea><wicri:noRegion>54290 Trier</wicri:noRegion><orgName type="university">Université de Trèves</orgName><placeName><settlement type="city">Trèves (Allemagne)</settlement><region type="land" nuts="1">Rhénanie-Palatinat</region></placeName></affiliation></author><author><name sortKey="Muller, Claude P" sort="Muller, Claude P" uniqKey="Muller C" first="Claude P" last="Muller">Claude P. Muller</name><affiliation wicri:level="4"><nlm:affiliation>Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, Esch-sur-Alzette, 4354 Grand-Duchy of Luxembourg ; Department of Immunology, Research Institute of Psychobiology, University of Trier, 54290 Trier, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, Esch-sur-Alzette, 4354 Grand-Duchy of Luxembourg ; Department of Immunology, Research Institute of Psychobiology, University of Trier, 54290 Trier</wicri:regionArea><wicri:noRegion>54290 Trier</wicri:noRegion><orgName type="university">Université de Trèves</orgName><placeName><settlement type="city">Trèves (Allemagne)</settlement><region type="land" nuts="1">Rhénanie-Palatinat</region></placeName></affiliation></author><author><name sortKey="Turner, Jonathan D" sort="Turner, Jonathan D" uniqKey="Turner J" first="Jonathan D" last="Turner">Jonathan D. Turner</name><affiliation wicri:level="1"><nlm:affiliation>Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, Esch-sur-Alzette, 4354 Grand-Duchy of Luxembourg.</nlm:affiliation><country xml:lang="fr">Luxembourg (pays)</country><wicri:regionArea>Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, Esch-sur-Alzette</wicri:regionArea><wicri:noRegion>Esch-sur-Alzette</wicri:noRegion></affiliation></author></analytic><series><title level="j">Clinical epigenetics</title><idno type="ISSN">1868-7075</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Blood Pressure (genetics)</term><term>Blood Pressure (physiology)</term><term>DNA Methylation</term><term>Female</term><term>Genetic Variation (genetics)</term><term>Genetic Variation (physiology)</term><term>Genotype</term><term>Haplotypes (genetics)</term><term>Humans</term><term>Hydrocortisone (analysis)</term><term>Hydrocortisone (physiology)</term><term>Male</term><term>Promoter Regions, Genetic (genetics)</term><term>Receptors, Glucocorticoid (genetics)</term><term>Receptors, Glucocorticoid (physiology)</term><term>Saliva (chemistry)</term><term>Stress, Psychological (genetics)</term><term>Stress, Psychological (physiopathology)</term><term>Young Adult</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Hydrocortisone</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Saliva</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Blood Pressure</term><term>Genetic Variation</term><term>Haplotypes</term><term>Promoter Regions, Genetic</term><term>Receptors, Glucocorticoid</term><term>Stress, Psychological</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Blood Pressure</term><term>Genetic Variation</term><term>Hydrocortisone</term><term>Receptors, Glucocorticoid</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Stress, Psychological</term></keywords><keywords scheme="MESH" xml:lang="en"><term>DNA Methylation</term><term>Female</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Young Adult</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Gender, genetic makeup, and prior experience interact to determine physiological responses to an external perceived stressor. Here, we investigated the contribution of both genetic variants and promoter methylation of the NR3C1 (glucocorticoid receptor) gene to the cardiovascular and hypothalamus-pituitary-adrenal (HPA) axis response to the socially evaluated cold pressor test (seCPT).</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26823689</PMID><DateCreated><Year>2016</Year><Month>01</Month><Day>29</Day></DateCreated><DateCompleted><Year>2016</Year><Month>04</Month><Day>22</Day></DateCompleted><DateRevised><Year>2016</Year><Month>01</Month><Day>29</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1868-7075</ISSN><JournalIssue CitedMedium="Print"><Volume>8</Volume><PubDate><Year>2016</Year></PubDate></JournalIssue><Title>Clinical epigenetics</Title><ISOAbbreviation>Clin Epigenetics</ISOAbbreviation></Journal><ArticleTitle>The cardiovascular and hypothalamus-pituitary-adrenal axis response to stress is controlled by glucocorticoid receptor sequence variants and promoter methylation.</ArticleTitle><Pagination><MedlinePgn>12</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1186/s13148-016-0180-y</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Gender, genetic makeup, and prior experience interact to determine physiological responses to an external perceived stressor. Here, we investigated the contribution of both genetic variants and promoter methylation of the NR3C1 (glucocorticoid receptor) gene to the cardiovascular and hypothalamus-pituitary-adrenal (HPA) axis response to the socially evaluated cold pressor test (seCPT).</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Two hundred thirty-two healthy participants were recruited and underwent the experiment. They were randomly assigned to either the seCPT group (cold water) or a control group (warm water). The seCPT group had a clear stress reaction; salivary cortisol levels and peak systolic and diastolic blood pressure all increased significantly compared to the control group. GR genotype (TthIIII, NR3C1-I, 1H, E22E, R23K, BclI and 9beta) and methylation data were obtained from 218 participants. Haplotypes were built from the GR genotypes, and haplotype 2 (minor allele of BclI) carriers had a higher cortisol response to the seCPT in comparison to non-carriers (20.77 ± 13.22; 14.99 ± 8.42; p = 0.034), as well as independently of the experimental manipulation, higher baseline heart rate (72.44 ± 10.99; 68.74 ± 9.79; p = 0.022) and blood pressure (115.81 ± 10.47; 111.61 ± 10.74; p = 0.048). Average methylation levels throughout promoter 1F and 1H were low (2.76 and 1.69 %, respectively), but there was a strong correlation between individual CpGs and the distance separating them (Pearson's correlation r = 0.725, p = 3.03 × 10(-26)). Higher promoter-wide methylation levels were associated with decreased baseline blood pressure, and when incorporated into a linear mixed effect model significantly predicted lower systolic and diastolic blood pressure evolution over time in response to the experimental manipulation. The underlying genotype significantly predicted methylation levels; particularly, the homozygous BclI minor allele was associated with higher methylation in promoter 1H (p = 0.042).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">This is one of the first studies linking epigenetic modifications of the GR promoter, receptor genotype and physiological measures of the stress response. At baseline, there were clear genetic and epigenetic effects on blood pressure. The seCPT induced a strong cardiovascular and HPA axis response, and both systems were affected by the functional genetic variants, although methylation also predicted blood pressure reactivity. The return to baseline was predominantly influenced by the genomic sequence. Overall, the physiological response to the seCPT is controlled by an exquisite mix of genetic and epigenetic factors.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li-Tempel</LastName><ForeName>Ting</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Neurobehavioral Genetics, Research Institute of Psychobiology, University of Trier, 54290 Trier, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Larra</LastName><ForeName>Mauro F</ForeName><Initials>MF</Initials><AffiliationInfo><Affiliation>Department of Clinical Physiology, Research Institute of Psychobiology, University of Trier, 54290 Trier, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sandt</LastName><ForeName>Estelle</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, Esch-sur-Alzette, 4354 Grand-Duchy of Luxembourg.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mériaux</LastName><ForeName>Sophie B</ForeName><Initials>SB</Initials><AffiliationInfo><Affiliation>Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, Esch-sur-Alzette, 4354 Grand-Duchy of Luxembourg.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schote</LastName><ForeName>Andrea B</ForeName><Initials>AB</Initials><AffiliationInfo><Affiliation>Department of Neurobehavioral Genetics, Research Institute of Psychobiology, University of Trier, 54290 Trier, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schächinger</LastName><ForeName>Hartmut</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Clinical Physiology, Research Institute of Psychobiology, University of Trier, 54290 Trier, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Muller</LastName><ForeName>Claude P</ForeName><Initials>CP</Initials><AffiliationInfo><Affiliation>Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, Esch-sur-Alzette, 4354 Grand-Duchy of Luxembourg ; Department of Immunology, Research Institute of Psychobiology, University of Trier, 54290 Trier, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Turner</LastName><ForeName>Jonathan D</ForeName><Initials>JD</Initials><Identifier Source="ORCID">0000-0002-2760-1071</Identifier><AffiliationInfo><Affiliation>Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, Esch-sur-Alzette, 4354 Grand-Duchy of Luxembourg.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>01</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Clin Epigenetics</MedlineTA><NlmUniqueID>101516977</NlmUniqueID><ISSNLinking>1868-7075</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011965">Receptors, Glucocorticoid</NameOfSubstance></Chemical><Chemical><RegistryNumber>WI4X0X7BPJ</RegistryNumber><NameOfSubstance UI="D006854">Hydrocortisone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Transl Psychiatry. 2014;4:e368</RefSource><PMID Version="1">24594779</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Endocrinol. 2001 Aug;15(8):1381-95</RefSource><PMID Version="1">11463861</PMID></CommentsCorrections><CommentsCorrections 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Version="1">22076031</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D001794" MajorTopicYN="N">Blood Pressure</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019175" MajorTopicYN="Y">DNA Methylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014644" MajorTopicYN="N">Genetic Variation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006239" MajorTopicYN="N">Haplotypes</DescriptorName><QualifierName UI="Q000235" 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MajorTopicYN="N">Saliva</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013315" MajorTopicYN="N">Stress, Psychological</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4730588</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Alternative promoter</Keyword><Keyword MajorTopicYN="N">Glucocorticoid receptor</Keyword><Keyword MajorTopicYN="N">Methylation</Keyword><Keyword MajorTopicYN="N">Single nucleotide polymorphism</Keyword></KeywordList><GeneralNote Owner="NLM">Original DateCompleted: 20160129</GeneralNote></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>10</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>01</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>1</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>1</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>1</Month><Day>30</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26823689</ArticleId><ArticleId IdType="doi">10.1186/s13148-016-0180-y</ArticleId><ArticleId IdType="pii">180</ArticleId><ArticleId IdType="pmc">PMC4730588</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li><li>Luxembourg (pays)</li></country><region><li>Rhénanie-Palatinat</li></region><settlement><li>Trèves (Allemagne)</li></settlement><orgName><li>Université de Trèves</li></orgName></list><tree><country name="Allemagne"><region name="Rhénanie-Palatinat"><name sortKey="Li Tempel, Ting" sort="Li Tempel, Ting" uniqKey="Li Tempel T" first="Ting" last="Li-Tempel">Ting Li-Tempel</name></region><name sortKey="Larra, Mauro F" sort="Larra, Mauro F" uniqKey="Larra M" first="Mauro F" last="Larra">Mauro F. Larra</name><name sortKey="Muller, Claude P" sort="Muller, Claude P" uniqKey="Muller C" first="Claude P" last="Muller">Claude P. Muller</name><name sortKey="Sch Chinger, Hartmut" sort="Sch Chinger, Hartmut" uniqKey="Sch Chinger H" first="Hartmut" last="Sch Chinger">Hartmut Sch Chinger</name><name sortKey="Schote, Andrea B" sort="Schote, Andrea B" uniqKey="Schote A" first="Andrea B" last="Schote">Andrea B. Schote</name></country><country name="Luxembourg (pays)"><noRegion><name sortKey="Sandt, Estelle" sort="Sandt, Estelle" uniqKey="Sandt E" first="Estelle" last="Sandt">Estelle Sandt</name></noRegion><name sortKey="Meriaux, Sophie B" sort="Meriaux, Sophie B" uniqKey="Meriaux S" first="Sophie B" last="Mériaux">Sophie B. Mériaux</name><name sortKey="Turner, Jonathan D" sort="Turner, Jonathan D" uniqKey="Turner J" first="Jonathan D" last="Turner">Jonathan D. Turner</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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