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[兔输卵管蛋白“DPF-1”的初步研究]

[Preliminary studies on the rabbit oviductin "DPF-1"].

作者信息

Shen H, Liu C J, Gu Z, Lu J N, Cheng G X, Tso J K

机构信息

Shanghai Institute of Cell Biology, Chinese Academy of Sciences.

出版信息

Shi Yan Sheng Wu Xue Bao. 1996 Dec;29(4):403-12.

PMID:9772685
Abstract

Anti-rabbit 64 kDa oviductin (named Development Promoting Factor-1, DPF-1) antibody could inhibit totally the early development of mouse fertilised eggs cultured in the conditioned medium derived from the rabbit oviduct mucosa epithelial cells, revealed that DPF-1 synthesized and secreted from rabbit oviduct mucosa has a function to overcome the developmental block of early mouse embryos. It seems that DPF-1 consists of a group of polypeptide isoforms, since its isoelectric points are ranging from 7.2 to 8.1 (Fig. 3). The synthesis and secretion of DPF-1 was not dependent on either 17 beta-estradiol or progesterone (Fig. 7), it can pass through zona pellucida easily and associate tightly with the early embryonic cell membrane (Fig. 6). By using Western blotting method, we found that DPF-1 was not appeared in the tissues of liver, heart, lung, spleen, uterus, ovary, small intestine, skeleton muscle and brain, but in that of oviduct (Fig. 4): some DPF-1 homologous molecules were also revealed in the oviduct tissues of mouse and golden hamster, their apparent molecular weights were 32 kDa, 72 kDa in mouse, and 49 kDa, 68 kDa in golden hamster (Fig. 5). Results obtained from the in vivo anti-fertility experiment, namely to analyse the anti-fertility effect in adult female mice after active immunization with DPF-1, showed that the fertility decreased significantly as compared to those of controls (p < 0.01) (Table 1). DPF-1 and its in vivo "loss of function" evidence we obtained will encourage us to study the mechanism of DPF-1 in overcoming the developmental block of early embryos, and its role in transition from maternal to embryonic control of early development.

摘要

抗兔64 kDa输卵管蛋白(命名为发育促进因子-1,DPF-1)抗体能够完全抑制在源自兔输卵管黏膜上皮细胞的条件培养基中培养的小鼠受精卵的早期发育,这表明从兔输卵管黏膜合成并分泌的DPF-1具有克服小鼠早期胚胎发育阻滞的功能。DPF-1似乎由一组多肽异构体组成,因为其等电点范围为7.2至8.1(图3)。DPF-1的合成和分泌不依赖于17β-雌二醇或孕酮(图7),它能够轻易穿过透明带并与早期胚胎细胞膜紧密结合(图6)。通过蛋白质免疫印迹法,我们发现DPF-1在肝、心、肺、脾、子宫、卵巢、小肠、骨骼肌和脑的组织中未出现,但在输卵管组织中出现(图4):在小鼠和金黄仓鼠的输卵管组织中也发现了一些DPF-1同源分子,其表观分子量在小鼠中为32 kDa、72 kDa,在金黄仓鼠中为49 kDa、68 kDa(图5)。体内抗生育实验的结果,即分析用DPF-1主动免疫成年雌性小鼠后的抗生育效果,表明与对照组相比生育力显著下降(p < 0.01)(表1)。我们获得的DPF-1及其体内“功能丧失”证据将促使我们研究DPF-1克服早期胚胎发育阻滞的机制,以及其在早期发育从母体控制向胚胎控制转变中的作用。

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