Characterization of a Glucocorticoid Receptor Gene (GR, NR3C1) Promoter Polymorphism Reveals Functionality and Extends a Haplotype With Putative Clinical Relevance
Identifieur interne : 000543 ( PascalFrancis/Checkpoint ); précédent : 000542; suivant : 000544Characterization of a Glucocorticoid Receptor Gene (GR, NR3C1) Promoter Polymorphism Reveals Functionality and Extends a Haplotype With Putative Clinical Relevance
Auteurs : Robert Kumsta [Allemagne, Royaume-Uni] ; Dirk Moser [Allemagne] ; Fabian Streit [Allemagne] ; Jan Willem Koper [Pays-Bas] ; Jobst Meyer [Allemagne] ; Stefan Wüst [Allemagne]Source :
- American journal of medical genetics. Part B, Neuropsychiatric genetics [ 1552-4841 ] ; 2009.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Hyperactivity of the hypothalamus-pituitary-adrenal (HPA) axis has been associated with the etiology of major depression. One of the factors underlying altered glucocorticoid signaling might be variability of the glucocorticoid receptor gene (GR, NR3C1). GR polymorphisms have been associated with variability in glucocorticoid sensitivity and endocrine responses to psychosocial stress. Furthermore, a common GR SNP (rs10482605), located in the promoter region, has been associated with major depression. We performed functional characterization of this SNP in vitro using a reporter gene assay under different stimulation conditions. Furthermore, we genotyped 219 subjects previously genotyped for four common GR SNPs to further characterize GR haplotype structure. The minor C allele of the rs10482605 SNP showed reduced transcriptional activity under unstimulated conditions and under different stimulation conditions in two brain derived cell lines. Linkage analyses revealed that the rs10482605 SNP is in high linkage disequilibrium with a A/G SNP in exon 9beta (rs6198), associated with relative glucocorticoid resistance and increased GRbeta mRNA stability. We provide evidence that two functional GR SNPs in linkage disequilibrium are responsible for both regulation of GR expression and mRNA stability. This newly characterized haplotype could increase the risk for the development of stress related disorders, including major depression. © 2008 Wiley-Liss, Inc.
Affiliations:
- Allemagne, Pays-Bas, Royaume-Uni
- Bade-Wurtemberg, District de Karlsruhe, Hollande-Méridionale, Rhénanie-Palatinat
- Mannheim, Rotterdam, Trèves (Allemagne)
- Université de Trèves
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Pascal:09-0234243Le document en format XML
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<front><div type="abstract" xml:lang="en">Hyperactivity of the hypothalamus-pituitary-adrenal (HPA) axis has been associated with the etiology of major depression. One of the factors underlying altered glucocorticoid signaling might be variability of the glucocorticoid receptor gene (GR, NR3C1). GR polymorphisms have been associated with variability in glucocorticoid sensitivity and endocrine responses to psychosocial stress. Furthermore, a common GR SNP (rs10482605), located in the promoter region, has been associated with major depression. We performed functional characterization of this SNP in vitro using a reporter gene assay under different stimulation conditions. Furthermore, we genotyped 219 subjects previously genotyped for four common GR SNPs to further characterize GR haplotype structure. The minor C allele of the rs10482605 SNP showed reduced transcriptional activity under unstimulated conditions and under different stimulation conditions in two brain derived cell lines. Linkage analyses revealed that the rs10482605 SNP is in high linkage disequilibrium with a A/G SNP in exon 9beta (rs6198), associated with relative glucocorticoid resistance and increased GRbeta mRNA stability. We provide evidence that two functional GR SNPs in linkage disequilibrium are responsible for both regulation of GR expression and mRNA stability. This newly characterized haplotype could increase the risk for the development of stress related disorders, including major depression. © 2008 Wiley-Liss, Inc.</div>
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<s5>12</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Polimorfismo mononucleótido</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Haplotype</s0>
<s5>13</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Haplotype</s0>
<s5>13</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Haplotipo</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Pertinence</s0>
<s5>14</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Relevance</s0>
<s5>14</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Pertinencia</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Expression génique</s0>
<s5>15</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Gene expression</s0>
<s5>15</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Expresión genética</s0>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Hypothalamus</s0>
<s5>16</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Hypothalamus</s0>
<s5>16</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Hipotálamo</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Hypophyse</s0>
<s5>17</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Pituitary gland</s0>
<s5>17</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Hipófisis</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Surrénale</s0>
<s5>18</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Adrenal glands</s0>
<s5>18</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Suprarrenal</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Axe</s0>
<s5>19</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Axis</s0>
<s5>19</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Eje</s0>
<s5>19</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Stress</s0>
<s5>20</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Stress</s0>
<s5>20</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Estrés</s0>
<s5>20</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE"><s0>Récepteur de glucocorticoïde</s0>
<s4>INC</s4>
<s5>86</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Trouble de l'humeur</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Mood disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Trastorno humor</s0>
<s5>37</s5>
</fC07>
<fN21><s1>173</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
<affiliations><list><country><li>Allemagne</li>
<li>Pays-Bas</li>
<li>Royaume-Uni</li>
</country>
<region><li>Bade-Wurtemberg</li>
<li>District de Karlsruhe</li>
<li>Hollande-Méridionale</li>
<li>Rhénanie-Palatinat</li>
</region>
<settlement><li>Mannheim</li>
<li>Rotterdam</li>
<li>Trèves (Allemagne)</li>
</settlement>
<orgName><li>Université de Trèves</li>
</orgName>
</list>
<tree><country name="Allemagne"><region name="Rhénanie-Palatinat"><name sortKey="Kumsta, Robert" sort="Kumsta, Robert" uniqKey="Kumsta R" first="Robert" last="Kumsta">Robert Kumsta</name>
</region>
<name sortKey="Meyer, Jobst" sort="Meyer, Jobst" uniqKey="Meyer J" first="Jobst" last="Meyer">Jobst Meyer</name>
<name sortKey="Moser, Dirk" sort="Moser, Dirk" uniqKey="Moser D" first="Dirk" last="Moser">Dirk Moser</name>
<name sortKey="Streit, Fabian" sort="Streit, Fabian" uniqKey="Streit F" first="Fabian" last="Streit">Fabian Streit</name>
<name sortKey="Wust, Stefan" sort="Wust, Stefan" uniqKey="Wust S" first="Stefan" last="Wüst">Stefan Wüst</name>
<name sortKey="Wust, Stefan" sort="Wust, Stefan" uniqKey="Wust S" first="Stefan" last="Wüst">Stefan Wüst</name>
</country>
<country name="Royaume-Uni"><noRegion><name sortKey="Kumsta, Robert" sort="Kumsta, Robert" uniqKey="Kumsta R" first="Robert" last="Kumsta">Robert Kumsta</name>
</noRegion>
</country>
<country name="Pays-Bas"><region name="Hollande-Méridionale"><name sortKey="Koper, Jan Willem" sort="Koper, Jan Willem" uniqKey="Koper J" first="Jan Willem" last="Koper">Jan Willem Koper</name>
</region>
</country>
</tree>
</affiliations>
</record>
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