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- Author: Hong-Wei Wang x
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Fujian Collaborative Innovation Center for Exploitation and Utilization of Marine Biological Resources, Xiamen, China
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Fujian Collaborative Innovation Center for Exploitation and Utilization of Marine Biological Resources, Xiamen, China
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Fujian Collaborative Innovation Center for Exploitation and Utilization of Marine Biological Resources, Xiamen, China
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Department of Biology, East Carolina University, Greenville, North Carolina, USA
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Fujian Collaborative Innovation Center for Exploitation and Utilization of Marine Biological Resources, Xiamen, China
State-Province Joint Engineering Laboratory of Marine Bioproducts and Technology, Xiamen University, Xiamen, China
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Our previous study showed that the in vivo positive effects of 17α,20β-dihydroxy-4-pregnen-3-one (DHP), the major progestin in zebrafish, on early spermatogenesis was much stronger than the ex vivo ones, which may suggest an effect of DHP on the expression of gonadotropins. In our present study, we first observed that fshb and lhb mRNA levels in the pituitary of male adult zebrafish were greatly inhibited by 3 weeks exposure to 10nM estradiol (E2). However, an additional 24h 100nM DHP exposure not only reversed the E2-induced inhibition, but also significantly increased the expression of fshb and lhb mRNA. These stimulatory effects were also observed in male adult fish without E2 pretreatment, and a time course experiment showed that it took 24h for fshb and 12h for lhb to respond significantly. Because these stimulatory activities were partially antagonized by a nuclear progesterone receptor (Pgr) antagonist mifepristone, we generated a Pgr-knockout (pgr –/–) model using the TALEN technique. With and without DHP in vivo treatment, fshb and lhb mRNA levels of pgr –/– were significantly lower than those of pgr +/+. Furthermore, ex vivo treatment of pituitary fragments of pgr –/– with DHP stimulated lhb, but not fshb mRNA expression. Results from double-colored fluorescent in situ hybridization showed that pgr mRNA was expressed only in fshb-expressing cells. Taken together, our results indicated that DHP participated in the regulation of neuroendocrine control of reproduction in male zebrafish, and exerted a Pgr-mediated direct stimulatory effect on fshb mRNA at pituitary level.
The Research Institute for Children, Departments of Pediatrics and Genetics, Children's Hospital, 200 Henry Clay Avenue, Research and Education Building, Room 2211, New Orleans, Louisiana 70118, USA
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The Research Institute for Children, Departments of Pediatrics and Genetics, Children's Hospital, 200 Henry Clay Avenue, Research and Education Building, Room 2211, New Orleans, Louisiana 70118, USA
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The Research Institute for Children, Departments of Pediatrics and Genetics, Children's Hospital, 200 Henry Clay Avenue, Research and Education Building, Room 2211, New Orleans, Louisiana 70118, USA
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The Research Institute for Children, Departments of Pediatrics and Genetics, Children's Hospital, 200 Henry Clay Avenue, Research and Education Building, Room 2211, New Orleans, Louisiana 70118, USA
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The Research Institute for Children, Departments of Pediatrics and Genetics, Children's Hospital, 200 Henry Clay Avenue, Research and Education Building, Room 2211, New Orleans, Louisiana 70118, USA
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In this study, an insulinoma-associated antigen-1 (INSM1)-binding site in the proximal promoter sequence of the insulin gene was identified. The co-transfection of INSM1 with rat insulin I/II promoter-driven reporter genes exhibited a 40–50% inhibitory effect on the reporter activity. Mutational experiments were performed by introducing a substitution, GG to AT, into the INSM1 core binding site of the rat insulin I/II promoters. The mutated insulin promoter exhibited a three- to 20-fold increase in the promoter activity over the wild-type promoter in several insulinoma cell lines. Moreover, INSM1 overexpression exhibited no inhibitory effect on the mutated insulin promoter. Chromatin immunoprecipitation assays using βTC-1, mouse fetal pancreas, and Ad-INSM1-transduced human islets demonstrated that INSM1 occupies the endogenous insulin promoter sequence containing the INSM1-binding site in vivo. The binding of the INSM1 to the insulin promoter could suppress ∼50% of insulin message in human islets. The mechanism for transcriptional repression of the insulin gene by INSM1 is mediated through the recruitment of cyclin D1 and histone deacetylase-3 to the insulin promoter. Anti-INSM1 or anti-cyclin D1 morpholino treatment of fetal mouse pancreas enhances the insulin promoter activity. These data strongly support the view that INSM1 is a new zinc-finger transcription factor that modulates insulin gene transcription during early pancreas development.
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Department of Physiology and Pathophysiology, Institutes of Biomedical Sciences, Department of Endocrinology, Shanghai Medical College
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In this study, the effect of high glucose (HG) on endothelial progenitor cell (EPC) proliferation and its relationship with cyclins and reactive oxygen species (ROS) were investigated. Mouse EPCs were isolated from bone marrow using a magnetic activated cell-sorting system and cultured in the presence or absence of HG (30 mmol/l). We found that in the early stage of incubation (3 days), HG promoted cell proliferation, and increased the expressions of cdk2 and cyclin E, while in the late stage of culture (7 days) it inhibited cell proliferation and decreased the expressions of cdk2, cyclin E, and proliferating cell nuclear antigen (PCNA). Moreover, on the third day after incubation, HG significantly inhibited the apoptosis of EPCs, while in the late stage it markedly activated caspase-3 and promoted apoptosis. ROS generation in cells and maleic dialdehyde level in medium were significantly increased in HG group on the seventh day, whereas the expressions of superoxide dismutase and glutathione levels decreased. Tempol, a membrane-permeable radical scavenger, significantly inhibited ROS production in EPCs and partially reversed the HG-mediated inhibition of EPCs proliferation on the seventh day. We hypothesize that in the HG environment, the biphasic response of EPC proliferation may be related to the generation of ROS, which causes modulation of cyclins and cell cycle effect.
State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
Institute of Reproductive Sciences, Key Laboratory of Animal Reproduction and Germplasm Enhancement in Universities of Shandong, College of Animal Science and Technology, Qingdao Agricultural University, Qingdao, China
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Institute of Reproductive Sciences, Key Laboratory of Animal Reproduction and Germplasm Enhancement in Universities of Shandong, College of Animal Science and Technology, Qingdao Agricultural University, Qingdao, China
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State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
Institute of Reproductive Sciences, Key Laboratory of Animal Reproduction and Germplasm Enhancement in Universities of Shandong, College of Animal Science and Technology, Qingdao Agricultural University, Qingdao, China
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State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
Institute of Reproductive Sciences, Key Laboratory of Animal Reproduction and Germplasm Enhancement in Universities of Shandong, College of Animal Science and Technology, Qingdao Agricultural University, Qingdao, China
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As a fat storage organ, adipose tissue is distributed widely all over the body and is important for energy supply, body temperature maintenance, organ protection, immune regulation and so on. In humans, both underweight and overweight women find it hard to become pregnant, which suggests that appropriate fat storage can guarantee the female reproductive capacity. In fact, a large mass of adipose tissue distributes around the reproductive system both in the male and female. However, the functions of ovary fat pad (the nearest adipose tissue to ovary) are not known. In our study, we found that the ovary fat pad-removed female mice showed decreased fertility and less ovulated mature eggs. We further identified that only a small proportion of follicles developed to antral follicle, and many follicles were blocked at the secondary follicle stage. The overall secretion levels of estrogen and FSH were lower in the whole estrus cycle (especially at proestrus); however, the LH level was higher in ovary fat pad-removed mice than that in control groups. Moreover, the estrus cycle of ovary fat pad-removed mice showed significant disorder. Besides, the expression of FSH receptor decreased, but the LH receptor increased in ovary fat pad-removed mice. These results suggest that ovary fat pad is important for mouse reproduction.
The Endocrine Institute of China Medical University, Department of Endocrinology and Metabolism, The Liaoning Provincial Key Laboratory of Endocrine Diseases, Shenyang 110001, People's Republic of China
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The Endocrine Institute of China Medical University, Department of Endocrinology and Metabolism, The Liaoning Provincial Key Laboratory of Endocrine Diseases, Shenyang 110001, People's Republic of China
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The Endocrine Institute of China Medical University, Department of Endocrinology and Metabolism, The Liaoning Provincial Key Laboratory of Endocrine Diseases, Shenyang 110001, People's Republic of China
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The Endocrine Institute of China Medical University, Department of Endocrinology and Metabolism, The Liaoning Provincial Key Laboratory of Endocrine Diseases, Shenyang 110001, People's Republic of China
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The Endocrine Institute of China Medical University, Department of Endocrinology and Metabolism, The Liaoning Provincial Key Laboratory of Endocrine Diseases, Shenyang 110001, People's Republic of China
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The Endocrine Institute of China Medical University, Department of Endocrinology and Metabolism, The Liaoning Provincial Key Laboratory of Endocrine Diseases, Shenyang 110001, People's Republic of China
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The Endocrine Institute of China Medical University, Department of Endocrinology and Metabolism, The Liaoning Provincial Key Laboratory of Endocrine Diseases, Shenyang 110001, People's Republic of China
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The Endocrine Institute of China Medical University, Department of Endocrinology and Metabolism, The Liaoning Provincial Key Laboratory of Endocrine Diseases, Shenyang 110001, People's Republic of China
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The Endocrine Institute of China Medical University, Department of Endocrinology and Metabolism, The Liaoning Provincial Key Laboratory of Endocrine Diseases, Shenyang 110001, People's Republic of China
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The Endocrine Institute of China Medical University, Department of Endocrinology and Metabolism, The Liaoning Provincial Key Laboratory of Endocrine Diseases, Shenyang 110001, People's Republic of China
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The Endocrine Institute of China Medical University, Department of Endocrinology and Metabolism, The Liaoning Provincial Key Laboratory of Endocrine Diseases, Shenyang 110001, People's Republic of China
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The Endocrine Institute of China Medical University, Department of Endocrinology and Metabolism, The Liaoning Provincial Key Laboratory of Endocrine Diseases, Shenyang 110001, People's Republic of China
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Acute and excessive iodine supplementation leads to iodine-induced thyroid cytotoxicity. Excessive oxidative stress has been suggested to be one of the underlying mechanisms in the development of thyroid cytotoxicity. The aim of this study was to investigate whether vitamin E (VE), an important antioxidant, could ameliorate iodine-induced thyroid cytotoxicity. A goiter was induced in rats by feeding a low-iodine (LI) diet for 12 weeks. Involution of hyperplasia was obtained by administering a twofold physiological dose of iodine in feeding water with/without the supplementation of 25-, 50-, or 100-fold physiological dose of VE in the LI diet for 4 weeks. In iodine-supplemented rats, thyroid epithelial cell ultrastructure injuries remained and were more severe. Relative weights of iodine-induced involuting glands were significantly reduced compared with the goiter, but still higher than control. Immunohistochemistry indicated that the expression of 4-hydroxynonenal, 8-hydroxyguanine, peroxiredoxin 5, and CD68 in thyroid increased (P<0.01), whereas thioredoxin reductase 1 decreased (P<0.01). VE supplementation attenuated thyroid cytotoxicity induced by iodine. A 50-fold VE dose was optimal in attenuating twofold iodine-induced thyroid cytotoxicity. However, VE supplementation did not reduce the weight or relative weight of the iodine-induced involuting gland. These results show that excess iodine leads to thyroid damage and VE supplementation can partly ameliorate iodine-induced thyroid cytotoxicity.
