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) μg/mL compared to 150 (88–207) μg/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.
How to translate text using browser tools
1 March 2006
Birth defects and anti–heat shock protein 70 antibodies in early pregnancy
David F. Child,
Peter R. Hudson,
Claire Hunter-Lavin,
Sagarika Mukhergee,
Susnata China,
Clive P. Williams,
John H. H. Williams
ACCESS THE FULL ARTICLE
It is not available for individual sale.
This article is only available to subscribers.
It is not available for individual sale.
It is not available for individual sale.
<
Previous Article
|