Birth defects and anti-heat shock protein 70 antibodies in early pregnancy

被引:16
作者
Child, DF
Hudson, PR [1 ]
Hunter-Lavin, C
Mukhergee, S
China, S
Williams, CP
Williams, JHH
机构
[1] Maelor Gen Hosp, Dept Chem Pathol, Wrexham LL13 7TD, Wales
[2] Maelor Gen Hosp, Dept Med, Wrexham LL13 7TD, Wales
[3] Maelor Gen Hosp, Dept Obstet & Gynaecol, Wrexham LL13 7TD, Wales
[4] Univ Chester, Chester Ctr Stress Res, Chester CH1 4BJ, Cheshire, England
关键词
D O I
10.1379/CSC-130R1.1
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
It has been suggested that induction of the heat shock response in the mammalian embryo during the critical period of organogenesis can result in anatomical malformation. We measured serum heat shock protein 70 (Hsp70), anti-Hsp70, and anti-Hsp60 in samples taken from expectant mothers at 16 weeks gestation. Samples from women whose babies were born with a birth defect (n = 30) were compared with controls who gave birth to healthy babies (n = 46). Anti-Hsp70 levels were significantly elevated in patients who later gave birth to babies with cleft lip or palate or neurological abnormalities (n = 10): 260 (223-406) mu g/mL compared to 150 (88-207) mu g/mL in controls (P < 0.001). No significant differences were found in serum Hsp70 and anti-Hsp60 levels between cases and controls. This finding of increased maternal anti-Hsp70 in patients who later gave birth to babies with these abnormalities suggests a previous stressful event may have contributed to the pathogenesis. Further work is required to determine whether Hsp70 has a direct or indirect role in this pathogenesis or whether anti-Hsp70 is simply a marker of a prior increase in Hsp70 due to a physiological stress that itself resulted in the damage. This work is consistent with previous studies showing a buffering role for Hsps in evolution.
引用
收藏
页码:101 / 105
页数:5
相关论文
共 27 条
[1]   Stress (heat shock) proteins - Molecular chaperones in cardiovascular biology and disease [J].
Benjamin, IJ ;
McMillan, DR .
CIRCULATION RESEARCH, 1998, 83 (02) :117-132
[2]  
Campisi J, 2003, CELL STRESS CHAPERON, V8, P272, DOI 10.1379/1466-1268(2003)008<0272:SEHIAF>2.0.CO
[3]  
2
[4]   Oxidant regulation of gene expression and neural tube development: Insights gained from diabetic pregnancy on molecular causes of neural tube defects [J].
Chang, TI ;
Horal, M ;
Jain, SK ;
Wang, F ;
Patel, R ;
Loeken, MR .
DIABETOLOGIA, 2003, 46 (04) :538-545
[5]   Folate deficiency-induced oxidative stress and apoptosis are mediated via homocysteine-dependent overproduction of hydrogen peroxide and enhanced activation of NF-κB in human Hep G2 cells [J].
Chern, CL ;
Huang, RFS ;
Chen, YH ;
Cheng, JT ;
Liu, TZ .
BIOMEDICINE & PHARMACOTHERAPY, 2001, 55 (08) :434-442
[6]   CHIP activates HSF1 and confers protection against apoptosis and cellular stress [J].
Dai, Q ;
Zhang, CL ;
Wu, YX ;
McDonough, H ;
Whaley, RA ;
Godfrey, V ;
Li, HH ;
Madamanchi, N ;
Xu, W ;
Neckers, L ;
Cyr, D ;
Patterson, C .
EMBO JOURNAL, 2003, 22 (20) :5446-5458
[7]   FOLATE LEVELS AND NEURAL-TUBE DEFECTS - IMPLICATIONS FOR PREVENTION [J].
DALY, LE ;
KIRKE, PN ;
MOLLOY, A ;
WEIR, DG ;
SCOTT, JM .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1995, 274 (21) :1698-1702
[8]   EMBRYONIC STRESS HYPOTHESIS OF TERATOGENESIS [J].
GERMAN, J .
AMERICAN JOURNAL OF MEDICINE, 1984, 76 (02) :293-301
[9]   In vitro studies show that Hsp70 can be released by glia and that exogenous Hsp70 can enhance neuronal stress tolerance [J].
Guzhova, I ;
Kislyakova, K ;
Moskaliova, O ;
Fridlanskaya, I ;
Tytell, M ;
Cheetham, M ;
Margulis, B .
BRAIN RESEARCH, 2001, 914 (1-2) :66-73
[10]   Hsp70 release from peripheral blood mononuclear cells [J].
Hunter-Lavin, C ;
Davies, EL ;
Bacelar, MMFVG ;
Marshall, MJ ;
Andrew, SM ;
Williams, JHH .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2004, 324 (02) :511-517