Gene Expression Patterns Associated with Posttraumatic Stress Disorder Following Exposure to the World Trade Center Attacks

被引：218

作者：

Yehuda, Rachel ^{[1
,2
]}

Cai, Guiqing ^{[3
]}

Golier, Julia A. ^{[1
,2
]}

Sarapas, Casey ^{[1
,2
]}

Galea, Sandro ^{[4
]}

Ising, Marcus ^{[5
]}

Rein, Theo ^{[5
]}

Schmeidler, James ^{[1
,2
]}

Mueller-Myhsok, Bertram ^{[5
]}

Holsboer, Florian ^{[5
]}

Buxbaum, Joseph D. ^{[3
]}

机构：

[1] James J Peters Vet Affairs Med Ctr, Bronx, NY 10458 USA

[2] Mt Sinai Sch Med, Bronx, NY USA

[3] Mt Sinai Sch Med, New York, NY USA

[4] Univ Michigan, Ctr Social Epidemiol & Populat Hlth, Ann Arbor, MI 48109 USA

[5] Max Planck Inst Psychiat, D-80804 Munich, Germany

来源：

BIOLOGICAL PSYCHIATRY | 2009年 / 66卷 / 07期

基金：

美国国家卫生研究院;

关键词：

Childhood trauma; cortisol; gene expression; human FKBP5 protein; posttraumatic stress disorders; September 11 terrorist attacks; FKBP5; POLYMORPHISMS;

D O I：

10.1016/j.biopsych.2009.02.034

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Background: Although genetic risk factors for posttraumatic stress disorder (PTSD) in similarly traumatized cohorts can be confounded with risk for type of exposure, the primary risk for exposure to the 9/11 attack on New York City was proximity, allowing study of PTSD risk in a sample that is not confounded by exposure-related risk. Methods: Thirty-five Caucasians (15 with PTSD, stratified for exposure, age, and gender) were selected from a population-representative sample of persons exposed to the attack from which longitudinal data had been collected in four previous waves. Whole blood gene expression and cortisol levels were obtained. Results: Seventeen probe sets were differentially expressed in PTSD. Identified genes were generally involved in hypothalamic-pituitary-adrenal (HPA) axis, signal transduction, or brain and immune cell function. FKBP5, a modulator of glucocorticoid receptor (GR) sensitivity, showed reduced expression in PTSD, consistent with enhanced GR responsiveness. FKBP5 expression was predicted by cortisol when entered with PTSD severity in regression analysis. Quantitative polymerase chain reaction confirmed significant reductions in FKBP5. Also less expressed in PTSD were STAT5B, a direct inhibitor of GR, and major histocompatibility complex (MHC) Class II. Conclusions: Consistent with observations of HPA axis dysfunction in PTSD, several genes involved in glucocorticoid signaling are differentially expressed among those with current PTSD.

引用

页码：708 / 711

页数：4