Differences in apoptotic status in the bovine placentome between spontaneous and induced parturition.
We conducted this study to analyze apoptotic changes in the bovine placentome at spontaneous and induced parturition. Cows delivered i) after the administration of dexamethasone followed by prostaglandin F(2α) and estriol, ii) after the administration of prostaglandin F(2α) and estriol or iii) spontaneously. Prepartum changes in plasma progesterone and estradiol-17β concentrations were similar between spontaneous and induced parturition. Messenger RNA of BCL2-related protein A1 (BCL2A1), an antiapoptotic gene, was expressed by trophoblast binucleate cells and caruncular epithelial cells. Quantitative RT-PCR showed that the expression of BCL2A1 mRNA in cotyledonary and caruncular portions was significantly lower in spontaneous parturition than induced parturition. The expression of BCL2-associated X protein (BAX) mRNA, a proapoptotic gene, was significantly higher in cotyledons at spontaneous parturition than parturition induced without dexamethasone. Caspase-3 (CASP3) mRNA and pre-activated CASP3 protein were predominantly detected in caruncular epithelial cells regardless of how parturition proceeded. Activated CASP3 protein was found in trophoblast uninucleate cells and binucleate cells rather than caruncular epithelial cells. In spontaneous parturition, intense staining of activated CASP3 was detected in caruncular epithelial cells. Spontaneous and dexamethasone-induced parturition increased apoptotic cells in the placentome compared with parturition induced without dexamethasone. The number of binucleate cells was significantly decreased in spontaneous parturition. The present results suggest that although the clinical dose of dexamethasone induces apoptosis in the placentome at term, neither dexamethasone nor prostaglandin F(2α) evoke normal physiological changes in the placentome during delivery such as a change in the balance of apoptosis-related genes and disappearance of binucleate cells.
Animal Biotechnology Group, Animal Research Center, Hokkaido Research Organization, Hokkaido 081-0038, Japan. hirayama-hiroki@hro.or.jp
Hiroki
H
Hirayama
Koichi
K
Ushizawa
Toru
T
Takahashi
Ken
K
Sawai
Satoru
S
Moriyasu
Soichi
S
Kageyama
Ryotaro
R
Miura
Motozumi
M
Matsui
Shigeo
S
Fukuda
Akira
A
Naito
Takashi
T
Fujii
Akira
A
Minamihashi
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism*; D002417:Cattle / Q000502:physiology*; D048750:Cell Nucleus Division / Q000187:drug effects; D053144:Cell Nucleus Shape / Q000187:drug effects; D003907:Dexamethasone / Q000008:administration & dosage; D015237:Dinoprost / Q000008:administration & dosage; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D004964:Estriol / Q000008:administration & dosage; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D007751:Labor, Induced / Q000379:methods / Q000662:veterinary*; D010120:Oxytocics; D036801:Parturition / Q000097:blood / Q000187:drug effects*; D010920:Placenta / Q000166:cytology / Q000187:drug effects*; D018457:Placenta, Retained / Q000517:prevention & control; D011247:Pregnancy; D012333:RNA, Messenger / Q000378:metabolism; D014327:Trophoblasts / Q000187:drug effects / Q000378:metabolism
D051017:Apoptosis Regulatory Proteins; D010120:Oxytocics; D012333:RNA, Messenger; D003907:Dexamethasone; D015237:Dinoprost; D004964:Estriol