Increased cell death in rat blastocysts exposed to maternal diabetes in utero and to high glucose or tumor necrosis factor-alpha in vitro.
Increased cell death in rat blastocysts exposed to maternal diabetes in utero and to high glucose or tumor necrosis factor-alpha in vitro.
复制标题
在子宫内暴露于母体糖尿病和在体外暴露于高葡萄糖或肿瘤坏死因子-α 的大鼠囊胚中细胞死亡增加。
作者:
S. Pampfer;I. Vanderheyden;Jane E. McCracken;Jarmila Vesela;R. Hertogh
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.
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影响因子:
3.6
作者:
Paria,BC;Das,SK;Huet-Hudson,YM;Dey,SK
通讯作者:
Dey,SK
DOI:
--
发表时间:
1995
期刊:
Cancer research.
影响因子:
--
作者:
Sensibar,JA;Sutkowski,DM;Raffo,A;Buttyan,R;Griswold,MD;Sylvester,SR;Kozlowski,JM;Lee,C
通讯作者:
Lee,C
DOI:
--
发表时间:
1989
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Hunt,JS;Soares,MJ;Lei,MG;Smith,RN;Wheaton,D;Atherton,RA;Morrison,DC
通讯作者:
Morrison,DC
影响因子:
3.6
作者:
T. L. Brown;B. C. Moulton;D. Witte;D. Swertfeger;J. Harmony
通讯作者:
T. L. Brown;B. C. Moulton;D. Witte;D. Swertfeger;J. Harmony
影响因子:
3.6
作者:
Brison, DR;Schultz, RM
通讯作者:
Schultz, RM