Document Detail


Increased cell death in rat blastocysts exposed to maternal diabetes in utero and to high glucose or tumor necrosis factor-alpha in vitro.
MedLine Citation:
PMID:  9428419     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The morphogenetic function of the transient phase of cell death that occurs during blastocyst maturation is not known but it is thought that its regulation results from a delicate balance between survival and lethal signals in the uterine milieu. In this paper, we show that blastocysts from diabetic rats have a higher incidence of dead cells than control embryos. Differential lineage staining indicated that increased nuclear fragmentation occurred mainly in the inner cell mass. In addition, terminal transferase-mediated dUTP nick end labeling (TUNEL) demonstrated an increase in the incidence of non-fragmented DNA-damaged nuclei in these blastocysts. Analysis of the expression of clusterin, a gene associated with apoptosis, by quantitative reverse transcription-polymerase chain reaction detected an increase in the steady-state level of its transcripts in blastocysts from diabetic rats. In situ hybridization revealed that about half the cells identified as expressing clusterin mRNA exhibited signs of nuclear fragmentation. In vitro experiments demonstrated that high D-glucose increased nuclear fragmentation, TUNEL labeling and clusterin transcription. Tumor necrosis factor-alpha (TNF-alpha), a cytokine whose synthesis is up-regulated in the diabetic uterus, did not induce nuclear fragmentation nor clusterin expression but increased the incidence of TUNEL-positive nuclei. The data suggest that excessive cell death in the blastocyst, most probably resulting from the overstimulation of a basal suicidal program by such inducers as glucose and TNF-alpha, may be a contributing factor of the early embryopathy associated with maternal diabetes.
Authors:
S Pampfer; I Vanderheyden; J E McCracken; J Vesela; R De Hertogh
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  124     ISSN:  0950-1991     ISO Abbreviation:  Development     Publication Date:  1997 Dec 
Date Detail:
Created Date:  1998-02-02     Completed Date:  1998-02-02     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  4827-36     Citation Subset:  IM    
Affiliation:
Physiology of Reproduction Research Unit (OBST 5330) University of Louvain Medical School, Brussels, Belgium. pampfer@obst.ucl.ac.be
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MeSH Terms
Descriptor/Qualifier:
Animals
Blastocyst / cytology*,  drug effects
Cell Death / drug effects
Cell Nucleus / ultrastructure
Clusterin
DNA Fragmentation
Female
Glucose / pharmacology*
Glycoproteins / genetics
Male
Molecular Chaperones*
Pregnancy
Pregnancy in Diabetics*
RNA, Messenger
Rats
Tumor Necrosis Factor-alpha / pharmacology*
Chemical
Reg. No./Substance:
0/Clusterin; 0/Glycoproteins; 0/Molecular Chaperones; 0/RNA, Messenger; 0/Tumor Necrosis Factor-alpha; 50-99-7/Glucose

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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