Knudsen T B, Blackburn M R, Chinsky J M, Airhart M J, Kellems R E
Department of Anatomy, East Tennessee State University, James H. Quillen College of Medicine, Johnson City 37614.
Biol Reprod. 1991 Jan;44(1):171-84. doi: 10.1095/biolreprod44.1.171.
This study has determined the cellular site of adenosine deaminase (ADA) expression in the mouse during development from Days 5 through 13 (day vaginal plug was found = Day 0) of gestation. Developmental expression of ADA progressed in two overlapping phases defined genetically (maternal vs. embryonal) and according to region (decidual vs. placental). In the first phase, ADA enzyme activity increased almost 200-fold in the antimesometrial region (decidua capsularis + giant trophoblast cells) from Days 6 through 9 of gestation but remained low in the mesometrial region. Immunohistochemical staining revealed a major localization of ADA to the secondary decidua. In the second phase, ADA activity increased several-fold in the placenta (labyrinth + basal zones) from Days 9 through 13 of gestation but remained low in the embryo proper. Immunohistochemical staining revealed a major localization of ADA to secondary giant cells, spongiotrophoblast, and labyrinthine trophoblast. Regression of decidua capsularis and growth of the spongiotrophoblast population accounted for an antimesometrial to placental shift in both ADA enzyme activity and a 40-kDa immunoreactive protein band. To verify a shift from maternal to fetal expression, studies were performed with two strains of mice (ICR, Eday) homozygous for a different ADA isozyme (ADA-A, ADA-B). Blastocysts homozygous for Adab were transferred to the uterus of pseudopregnant female recipients homozygous for Adaa. The isozymic pattern in chimeric embryo-decidual units analyzed at Days 7, 9, 11, and 13 revealed a predominance of maternal-encoded enzyme at Days 7 through 11 of gestation and a shift to fetal-encoded enzyme by Day 13. Thus, maternal expression of ADA in the antimesometrial decidua may play a role during establishment of the embryo in the uterine environment, whereas fetal expression of ADA in the trophoblast might be important to placentation.
本研究确定了妊娠第5天至13天（发现阴道栓之日 = 第0天）期间小鼠体内腺苷脱氨酶（ADA）表达的细胞位点。ADA的发育性表达在两个重叠阶段进行，这两个阶段根据遗传（母体与胚胎）和区域（蜕膜与胎盘）来定义。在第一阶段，从妊娠第6天至第9天，抗中膜区域（包蜕膜 + 巨大滋养层细胞）的ADA酶活性增加了近200倍，但中膜区域的活性仍较低。免疫组织化学染色显示ADA主要定位于次级蜕膜。在第二阶段，从妊娠第9天至第13天，胎盘（迷路 + 基底层）中的ADA活性增加了几倍，但胚胎本身的活性仍较低。免疫组织化学染色显示ADA主要定位于次级巨细胞、海绵滋养层和迷路滋养层。包蜕膜的退化和海绵滋养层细胞群的生长导致了ADA酶活性和一条40 kDa免疫反应蛋白带在抗中膜到胎盘的转移。为了验证从母体表达向胎儿表达的转变，对两种纯合不同ADA同工酶（ADA-A、ADA-B）的小鼠品系（ICR、Eday）进行了研究。将纯合Adab的囊胚转移到纯合Adaa的假孕雌性受体子宫中。在第7、9、11和13天分析的嵌合胚胎 - 蜕膜单位中的同工酶模式显示，在妊娠第7天至第11天，母体编码的酶占主导，到第13天则转变为胎儿编码的酶。因此，抗中膜蜕膜中ADA的母体表达可能在胚胎在子宫环境中的着床过程中起作用，而滋养层中ADA的胎儿表达可能对胎盘形成很重要。
