Search Results
You are looking at 1 - 3 of 3 items for
- Author: Hua Mei x
- Refine by access: Content accessible to me x
Search for other papers by Hua Mei in
Google Scholar
PubMed
Search for other papers by Cara Walters in
Google Scholar
PubMed
Search for other papers by Richard Carter in
Google Scholar
PubMed
Search for other papers by William H Colledge in
Google Scholar
PubMed
Mice with mutations in the kisspeptin signaling pathway (Kiss1 −/− or Gpr54 −/− ) have low gonadotrophic hormone levels, small testes, and impaired spermatogenesis. Between 2 and 7 months of age, however, the testes of the mutant mice increase in weight and in Gpr54 −/− mice, the number of seminiferous tubules containing spermatids/spermatozoa increases from 17 to 78%. In contrast, the Kiss1 −/− mice have a less severe defect in spermatogenesis and larger testes than Gpr54 −/− mice at both 2 and 7 months of age. The reason for the improved spermatogenesis was investigated. Plasma testosterone and FSH levels did not increase with age in the mutant mice and remained much lower than in wild-type (WT) mice. In contrast, intratesticular testosterone levels were similar between mutant and WT mice. These data indicate that age-related spermatogenesis can be completed under conditions of low plasma testosterone and FSH and that intratesticular testosterone may contribute to this process. In addition, however, when the Gpr54 −/− mice were fed a phytoestrogen-free diet, they showed no age-related increase in testes weight or improved spermatogenesis. Thus, both genetic and environmental factors are involved in the improved spermatogenesis in the mutant mice as they age although the mice still remain infertile. These data show that the possible impact of dietary phytoestrogens should be taken into account when studying the phenotype of mutant mice with defects in the reproductive axis.
Search for other papers by Yan Xu in
Google Scholar
PubMed
Search for other papers by Miao Liu in
Google Scholar
PubMed
Search for other papers by Yi-hua Gu in
Google Scholar
PubMed
Search for other papers by Xiao-feng Jia in
Google Scholar
PubMed
Search for other papers by Yong-Mei Chen in
Google Scholar
PubMed
Search for other papers by Michelle Santos in
Google Scholar
PubMed
Search for other papers by Ai-Zhen Wu in
Google Scholar
PubMed
Search for other papers by Xiao-dong Zhang in
Google Scholar
PubMed
Medical School of Fudan University, Center for Biomedical Research, The Rockefeller University, National Population and Family Planning Key Laboratory of Contraceptive Drugs and Devices, Department of Anatomy, Shanghai, China
Search for other papers by Hui-Juan Shi in
Google Scholar
PubMed
Medical School of Fudan University, Center for Biomedical Research, The Rockefeller University, National Population and Family Planning Key Laboratory of Contraceptive Drugs and Devices, Department of Anatomy, Shanghai, China
Search for other papers by Ching-Ling C Chen in
Google Scholar
PubMed
With tetraspanning topology, members of the membrane-spanning four-domain subfamily A (MS4A) may facilitate signaling or ion channel functions in many tissues. In this study, we report the cloning of a full-length cDNA from rat testis, designated Ms4a14 (Sp3111), which encodes the MS4A protein with 1139 amino acid residues. In situ hybridization and immunohistochemical analyses indicate that Ms4a14 is predominantly expressed from round spermatids to spermatozoa at specific stages in the rat testis at both the mRNA and protein level. Immunofluorescence analysis revealed that MS4A14 (SP3111) is located in the acrosome and the midpiece of the flagellum in mature sperm. Previously, we explored and reported the involvement of MS4A14 in reproductive functions, using antibody blockage during IVF and a transgenic RNA interference method in a mouse model. Our results suggested that MS4A14 is involved in fertilization and zygote division. As MS4A14 protein exists in mammals, such as humans, cows, dogs, and rodents, MS4A14 may play a ubiquitous role in mammalian reproduction.
Search for other papers by Wang Han-zheng in
Google Scholar
PubMed
Search for other papers by Lu Shu-hua in
Google Scholar
PubMed
Search for other papers by Shen Wei-xiong in
Google Scholar
PubMed
Search for other papers by Sun Zhi-da in
Google Scholar
PubMed
Search for other papers by Zhou Wei in
Google Scholar
PubMed
Search for other papers by Wu Yu-fen in
Google Scholar
PubMed
Search for other papers by Zhou Mei-rong in
Google Scholar
PubMed
Summary. Cell suspensions were prepared from human corpora lutea obtained during the mid-luteal phase. Progesterone production was assessed after short-term incubation of luteal cell suspensions. Luteal cells were very sensitive to hCG, the concentration required for 50% maximum response being 0·01 i.u./ml, and the response was 5 times higher than the basal production.
Oestradiol (1–100 μm) induced a significant dose-related decrease in both basal and hCG-stimulated progesterone production. The A-nor steroidal compounds anordrin and AF-45 reduced hCG-stimulated progesterone production only at the high concentration of 100 μm. The ED50 values were approximately 3 μm, 75 μm and 100 μm for oestradiol, AF-45 and anordrin respectively. Anordrin showed no significant effects on basal progesterone production. In addition, oestradiol markedly inhibited the activity of 3β-hydroxysteroid dehydrogenase in luteal cells, expressed by the conversion of pregnenolone to progesterone, but the inhibitory effects of anordrin and AF-45 were negligible or relatively low.
The effects of anordrin and AF-45 were different from those of oestradiol on progesterone production by human luteal cells in vitro, indicating that neither substance is likely to be a useful luteolytic agent in women.
Keywords: A-nor steroid; oestradiol; luteal cells; progesterone; 3β-hydroxysteroid dehydrogenase; man
