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Auteur Xiang LI |
Documents disponibles écrits par cet auteur (2)
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Developmental vitamin D deficiency increases foetal exposure to testosterone / Asad Amanat ALI in Molecular Autism, 11 (2020)
[article]
Titre : Developmental vitamin D deficiency increases foetal exposure to testosterone Type de document : Texte imprimé et/ou numérique Auteurs : Asad Amanat ALI, Auteur ; Xiaoying CUI, Auteur ; Renata Aparecida Nedel PERTILE, Auteur ; Xiang LI, Auteur ; Gregory MEDLEY, Auteur ; Suzanne Adele ALEXANDER, Auteur ; Andrew J. O. WHITEHOUSE, Auteur ; John Joseph MCGRATH, Auteur ; Darryl Walter EYLES, Auteur Langues : Anglais (eng) Mots-clés : Animal model Aromatase Autism Developmental vitamin D deficiency Methylation Testosterone Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders which are more common in males. The 'prenatal sex steroid' hypothesis links excessive sex-steroid exposure during foetal life with the behavioural differences observed in ASD. However, the reason why sex steroid exposure may be excessive remains unclear. Epidemiological studies have identified several environmental risk factors associated with ASD, including developmental vitamin D (DVD) deficiency. We have demonstrated in an animal model that DVD-deficiency is associated with a hyper-inflammatory response in placentas from male but not female foetuses. Vitamin D also regulates the expression of several steroidogenic enzymes in vitro. Therefore using this animal model, we have examined whether DVD-deficiency leads to increased sex-steroid levels in both the maternal and foetal compartments. METHODS: Female rats are fed a vitamin D deficient diet from 6 weeks before mating until tissue collection at embryonic day 18. We examined the levels of testosterone, androstenedione and corticosterone in maternal plasma, foetal brains and amniotic fluid. We further examined gene expressions of steroidogenic enzymes and DNA methylation of aromatase promoters in foetal brains as a potential molecular mechanism regulating testosterone expression. RESULTS: We show that DVD-deficiency increases testosterone levels in maternal blood. We also show elevated levels of testosterone and androstenedione in the amniotic fluid of female but not male DVD-deficient foetuses. Testosterone levels were also elevated in DVD-deficient male brains. Vitamin D, like other steroid-related hormones, regulates gene expression via methylation. Therefore we examined whether the significant elevation in testosterone in male brains was due to such a potential gene-silencing mechanism. We show that the promoter of aromatase was hyper-methylated compared to male controls. LIMITATIONS: A reduction in aromatase, in addition to causing excessive testosterone, could also lead to a reduction in estradiol which was not examined here. CONCLUSIONS: This study is the first to show how an epidemiologically established environmental risk factor for ASD may selectively elevate testosterone in male embryonic brains. These findings provide further mechanistic support for the prenatal sex steroid theory of ASD. En ligne : http://dx.doi.org/10.1186/s13229-020-00399-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438
in Molecular Autism > 11 (2020)[article] Developmental vitamin D deficiency increases foetal exposure to testosterone [Texte imprimé et/ou numérique] / Asad Amanat ALI, Auteur ; Xiaoying CUI, Auteur ; Renata Aparecida Nedel PERTILE, Auteur ; Xiang LI, Auteur ; Gregory MEDLEY, Auteur ; Suzanne Adele ALEXANDER, Auteur ; Andrew J. O. WHITEHOUSE, Auteur ; John Joseph MCGRATH, Auteur ; Darryl Walter EYLES, Auteur.
Langues : Anglais (eng)
in Molecular Autism > 11 (2020)
Mots-clés : Animal model Aromatase Autism Developmental vitamin D deficiency Methylation Testosterone Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders which are more common in males. The 'prenatal sex steroid' hypothesis links excessive sex-steroid exposure during foetal life with the behavioural differences observed in ASD. However, the reason why sex steroid exposure may be excessive remains unclear. Epidemiological studies have identified several environmental risk factors associated with ASD, including developmental vitamin D (DVD) deficiency. We have demonstrated in an animal model that DVD-deficiency is associated with a hyper-inflammatory response in placentas from male but not female foetuses. Vitamin D also regulates the expression of several steroidogenic enzymes in vitro. Therefore using this animal model, we have examined whether DVD-deficiency leads to increased sex-steroid levels in both the maternal and foetal compartments. METHODS: Female rats are fed a vitamin D deficient diet from 6 weeks before mating until tissue collection at embryonic day 18. We examined the levels of testosterone, androstenedione and corticosterone in maternal plasma, foetal brains and amniotic fluid. We further examined gene expressions of steroidogenic enzymes and DNA methylation of aromatase promoters in foetal brains as a potential molecular mechanism regulating testosterone expression. RESULTS: We show that DVD-deficiency increases testosterone levels in maternal blood. We also show elevated levels of testosterone and androstenedione in the amniotic fluid of female but not male DVD-deficient foetuses. Testosterone levels were also elevated in DVD-deficient male brains. Vitamin D, like other steroid-related hormones, regulates gene expression via methylation. Therefore we examined whether the significant elevation in testosterone in male brains was due to such a potential gene-silencing mechanism. We show that the promoter of aromatase was hyper-methylated compared to male controls. LIMITATIONS: A reduction in aromatase, in addition to causing excessive testosterone, could also lead to a reduction in estradiol which was not examined here. CONCLUSIONS: This study is the first to show how an epidemiologically established environmental risk factor for ASD may selectively elevate testosterone in male embryonic brains. These findings provide further mechanistic support for the prenatal sex steroid theory of ASD. En ligne : http://dx.doi.org/10.1186/s13229-020-00399-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438 Longitudinal relations among family dysfunction, depressive symptoms, and cyberbullying involvement in Chinese early adolescents: Disentangling between- and within-person associations / Jianhua ZHOU in Development and Psychopathology, 36-1 (February 2024)
[article]
Titre : Longitudinal relations among family dysfunction, depressive symptoms, and cyberbullying involvement in Chinese early adolescents: Disentangling between- and within-person associations Type de document : Texte imprimé et/ou numérique Auteurs : Jianhua ZHOU, Auteur ; Xiang LI, Auteur ; Yan ZOU, Auteur ; Xue GONG, Auteur Article en page(s) : p.395-403 Langues : Anglais (eng) Mots-clés : cyberbullying cybervictimization depressive symptoms family dysfunction Index. décimale : PER Périodiques Résumé : Family dysfunction plays an important role in cyberbullying and cybervictimization. However, little research has investigated the longitudinal relations and the mediating mechanisms between them during adolescence. This study examined the longitudinal relations between family dysfunction and cyberbullying and cybervictimization, along with whether depressive symptoms function as mediators between them at the within-person level. A total of 3,743 Chinese adolescents (46.2% females; Mage = 9.92 years; SD = 0.51) participated a five-wave longitudinal study with a 6-month time interval. The results of random intercept cross-lagged panel model found that: (1) family dysfunction directly predicted depressive symptoms and vice versa at the within-person level; (2) depressive symptoms directly predicted cyberbullying and cybervictimization at the within-person level, but not vice versa; (3) family dysfunction indirectly predicted cyberbullying and cybervictimization via depressive symptoms at the within-person level; (4) at the between-person level, there were significant associations among family dysfunction, depressive symptoms, cyberbullying and cybervictimization. The results are discussed on the basis of the mechanisms that lead to cyberbullying and cybervictimization. En ligne : https://dx.doi.org/10.1017/S0954579422001274 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=523
in Development and Psychopathology > 36-1 (February 2024) . - p.395-403[article] Longitudinal relations among family dysfunction, depressive symptoms, and cyberbullying involvement in Chinese early adolescents: Disentangling between- and within-person associations [Texte imprimé et/ou numérique] / Jianhua ZHOU, Auteur ; Xiang LI, Auteur ; Yan ZOU, Auteur ; Xue GONG, Auteur . - p.395-403.
Langues : Anglais (eng)
in Development and Psychopathology > 36-1 (February 2024) . - p.395-403
Mots-clés : cyberbullying cybervictimization depressive symptoms family dysfunction Index. décimale : PER Périodiques Résumé : Family dysfunction plays an important role in cyberbullying and cybervictimization. However, little research has investigated the longitudinal relations and the mediating mechanisms between them during adolescence. This study examined the longitudinal relations between family dysfunction and cyberbullying and cybervictimization, along with whether depressive symptoms function as mediators between them at the within-person level. A total of 3,743 Chinese adolescents (46.2% females; Mage = 9.92 years; SD = 0.51) participated a five-wave longitudinal study with a 6-month time interval. The results of random intercept cross-lagged panel model found that: (1) family dysfunction directly predicted depressive symptoms and vice versa at the within-person level; (2) depressive symptoms directly predicted cyberbullying and cybervictimization at the within-person level, but not vice versa; (3) family dysfunction indirectly predicted cyberbullying and cybervictimization via depressive symptoms at the within-person level; (4) at the between-person level, there were significant associations among family dysfunction, depressive symptoms, cyberbullying and cybervictimization. The results are discussed on the basis of the mechanisms that lead to cyberbullying and cybervictimization. En ligne : https://dx.doi.org/10.1017/S0954579422001274 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=523