Apoptosis and related proteins in placenta of intrauterine fetal death in prostaglandin f receptor-deficient mice.
The present study investigated whether the increase of apoptosis in the placenta is associated with intrauterine fetal death in prostaglandin F receptor-deficient mice. Apoptosis was demonstrated within placental and decidual tissue by the TUNEL method. The majority of apoptosis was found in syncytiotrophoblast tissues. Enhanced TUNEL-positive staining in the syncytiotrophoblast layer was scattered in the placental tissues in clusters of apoptotic cells in the death group. Marked TUNEL-positive cells were identified in decidua of both groups. The rate of apoptosis in the placenta and decidua in the death group was higher than that in the survival group (P < 0.05). Immunohistochemical analysis showed that the level of active caspase-3 protein expression in the placenta in the death group was much higher than that in the survival group. The level of Bcl-2 protein expression in the placenta in the death group was much lower than that in the survival group. Western blot analysis demonstrated that increased expression of the active form of caspase-3 was detected in the placenta and decidua in the death group compared with that in the survival group. In contrast, a decrease in the expression of Bcl-2 was detected in the placenta and decidua in the death group compared with that in the survival group. Enhanced expression of Bax:Bcl-2 ratio was detected in placenta and decidua in the death group compared with that in the survival group. Thus, significantly increased apoptosis in the mouse placenta and decidua might be involved in the pathophysiologic mechanism of intrauterine fetal death.
Mu
Junwu
J
Department of Obstetrics and Gynecology, Osaka University, Faculty of Medicine, Osaka, Japan. mujunwu@hotmail.com
Kanzaki
Toru
T
Si
Xiaoe
X
Tomimatsu
Takuji
T
Fukuda
Hirotsugu
H
Shioji
Mitsnori
M
Murata
Yuji
Y
Sugimoto
Yukihiko
Y
Ichikawa
Atsushi
A
D000818:Animals; D017209:Apoptosis / Q000235:genetics* / Q000502:physiology*; D015153:Blotting, Western; D053148:Caspase 3; D020169:Caspases / Q000096:biosynthesis / Q000235:genetics; D015237:Dinoprost / Q000378:metabolism; D005260:Female; D005313:Fetal Death / Q000235:genetics* / Q000473:pathology*; D019254:Genes, bcl-2 / Q000235:genetics; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D020287:In Situ Nick-End Labeling; D051379:Mice; D018345:Mice, Knockout; D011247:Pregnancy; D011257:Pregnancy Proteins / Q000235:genetics* / Q000378:metabolism*; D014176:Protein Biosynthesis; D011506:Proteins / Q000235:genetics*; D011518:Proto-Oncogene Proteins / Q000235:genetics; D019253:Proto-Oncogene Proteins c-bcl-2; D011982:Receptors, Prostaglandin / Q000235:genetics* / Q000502:physiology*; D051028:bcl-2-Associated X Protein
C494827:Bax protein, mouse; D011257:Pregnancy Proteins; D011506:Proteins; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D011982:Receptors, Prostaglandin; D051028:bcl-2-Associated X Protein; C034671:prostaglandin F2alpha receptor; D015237:Dinoprost; C505409:Casp3 protein, mouse; D053148:Caspase 3; D020169:Caspases