2009
Dynamic DNA methylation programs persistent adverse effects of early-life stress
MURGATROYD, Chris; Alexandre V PATCHEV; Yonghe WU; Vincenzo MICALE; Yvonne BOCKMUHL et al.Základní údaje
Originální název
Dynamic DNA methylation programs persistent adverse effects of early-life stress
Autoři
MURGATROYD, Chris; Alexandre V PATCHEV; Yonghe WU; Vincenzo MICALE; Yvonne BOCKMUHL; Dieter FISCHER; Florian HOLSBOER; Carsten T WOTJAK; Osborne F X ALMEIDA a Dietmar SPENGLER
Vydání
Nature Neuroscience, NEW YORK, NATURE PUBLISHING GROUP, 2009, 1097-6256
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
30000 3. Medical and Health Sciences
Stát vydavatele
Spojené státy
Utajení
není předmětem státního či obchodního tajemství
Impakt faktor
Impact factor: 14.345
Označené pro přenos do RIV
Ne
UT WoS
Klíčová slova anglicky
PITUITARY-ADRENAL AXIS; GENE-EXPRESSION; MOUSE MODEL; EPIGENETIC REGULATION; BDNF TRANSCRIPTION; RETT-SYNDROME; DISORDERS; ANXIETY; MECP2; BRAIN
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 7. 8. 2012 08:20, Olga Křížová
Anotace
V originále
Adverse early life events can induce long-lasting changes in physiology and behavior. We found that early-life stress (ELS) in mice caused enduring hypersecretion of corticosterone and alterations in passive stress coping and memory. This phenotype was accompanied by a persistent increase in arginine vasopressin (AVP) expression in neurons of the hypothalamic paraventricular nucleus and was reversed by an AVP receptor antagonist. Altered Avp expression was associated with sustained DNA hypomethylation of an important regulatory region that resisted age-related drifts in methylation and centered on those CpG residues that serve as DNA-binding sites for the methyl CpG-binding protein 2 (MeCP2). We found that neuronal activity controlled the ability of MeCP2 to regulate activity-dependent transcription of the Avp gene and induced epigenetic marking. Thus, ELS can dynamically control DNA methylation in postmitotic neurons to generate stable changes in Avp expression that trigger neuroendocrine and behavioral alterations that are frequent features in depression.