Search Results
You are looking at 1 - 2 of 2 items for
- Author: Guang-Yi Sun x
- Refine by Access: All content x
Search for other papers by Dong Zhang in
Google Scholar
PubMed
Search for other papers by Shen Yin in
Google Scholar
PubMed
Search for other papers by Man-Xi Jiang in
Google Scholar
PubMed
Search for other papers by Wei Ma in
Google Scholar
PubMed
Search for other papers by Yi Hou in
Google Scholar
PubMed
Search for other papers by Cheng-Guang Liang in
Google Scholar
PubMed
Search for other papers by Ling-Zhu Yu in
Google Scholar
PubMed
Search for other papers by Wei-Hua Wang in
Google Scholar
PubMed
Search for other papers by Qing-Yuan Sun in
Google Scholar
PubMed
The present study was designed to investigate the localization and function of cytoplasmic dynein (dynein) during mouse oocyte meiosis and its relationship with two major spindle checkpoint proteins, mitotic arrest-deficient (Mad) 1 and Mad2. Oocytes at various stages during the first meiosis were fixed and immunostained for dynein, Mad1, Mad2, kinetochores, microtubules, and chromosomes. Some oocytes were treated with nocodazole before examination. Anti-dynein antibody was injected into the oocytes at germinal vesicle (GV) stage before the examination of its effects on meiotic progression or Mad1 and Mad2 localization. Results showed that dynein was present in the oocytes at various stages from GV to metaphase II and the locations of Mad1 and Mad2 were associated with dynein’s movement. Both Mad1 and Mad2 had two existing states: one existed in the cytoplasm (cytoplasmic Mad1 or cytoplasmic Mad2), which did not bind to kinetochores, while the other bound to kinetochores (kinetochore Mad1 or kinetochore Mad2). The equilibrium between the two states varied during meiosis and/or in response to the changes of the connection between microtubules and kinetochores. Cytoplasmic Mad1 and Mad2 recruited to chromosomes when the connection between microtubules and chromosomes was destroyed. Inhibition of dynein interferes with cytoplasmic Mad1 and Mad2 transportation from chromosomes to spindle poles, thus inhibits checkpoint silence and delays anaphase onset. These results indicate that dynein may play a role in spindle checkpoint inactivation.
Search for other papers by Hong-Jie Yuan in
Google Scholar
PubMed
Search for other papers by Zhi-Bin Li in
Google Scholar
PubMed
Search for other papers by Xin-Yue Zhao in
Google Scholar
PubMed
Search for other papers by Guang-Yi Sun in
Google Scholar
PubMed
Search for other papers by Guo-Liang Wang in
Google Scholar
PubMed
Search for other papers by Ying-Qi Zhao in
Google Scholar
PubMed
Search for other papers by Min Zhang in
Google Scholar
PubMed
Search for other papers by Jing-He Tan in
Google Scholar
PubMed
Mechanisms by which female stress and particularly glucocorticoids impair oocyte competence are largely unclear. Although one study demonstrated that glucocorticoids triggered apoptosis in ovarian cells and oocytes by activating the FasL/Fas system, other studies suggested that they might induce apoptosis through activating other signaling pathways as well. In this study, both in vivo and in vitro experiments were conducted to test the hypothesis that glucocorticoids might trigger apoptosis in oocytes and ovarian cells through activating the TNF-α system. The results showed that cortisol injection of female mice (1.) impaired oocyte developmental potential and mitochondrial membrane potential with increased oxidative stress; (2.) induced apoptosis in mural granulosa cells (MGCs) with increased oxidative stress in the ovary; and (3.) activated the TNF-α system in both ovaries and oocytes. Culture with corticosterone induced apoptosis and activated the TNF-α system in MGCs. Knockdown or knockout of TNF-α significantly ameliorated the pro-apoptotic effects of glucocorticoids on oocytes and MGCs. However, culture with corticosterone downregulated TNF-α expression significantly in oviductal epithelial cells. Together, the results demonstrated that glucocorticoids impaired oocyte competence and triggered apoptosis in ovarian cells through activating the TNF-α system and that the effect of glucocorticoids on TNF-α expression might vary between cell types.
