Search Results
You are looking at 1 - 10 of 30 items for
- Author: Yang Yan x
- Refine by access: All content x
Search for other papers by Xiang Xiao in
Google Scholar
PubMed
Search for other papers by Yue Yang in
Google Scholar
PubMed
Search for other papers by Baiping Mao in
Google Scholar
PubMed
Search for other papers by C Yan Cheng in
Google Scholar
PubMed
Search for other papers by Ya Ni in
Google Scholar
PubMed
SRC family kinases (SFKs) are known regulators of multiple cellular events, including cell movement, differentiation, proliferation, survival and apoptosis. SFKs are expressed virtually by all mammalian cells. They are non-receptor protein kinases that phosphorylate a variety of cellular proteins on tyrosine, leading to the activation of protein targets in response to environmental stimuli. Among SFKs, SRC, YES and FYN are the ubiquitously expressed and best studied members. In fact, SRC, the prototypical SFK, was the first tyrosine kinase identified in mammalian cells. Studies have shown that SFKs are regulators of cell junctions, and function in endocytosis and membrane trafficking to regulate junction restructuring events. Herein, we briefly summarize the recent findings in the field regarding the role of SFKs in the testis in regulating spermatogenesis, particularly in Sertoli–Sertoli and Sertoli–germ cell adhesion. While it is almost 50 years since the identification of the oncogene v-Src encoded by Rous sarcoma transforming virus, the understanding of SFK involvement during spermatogenesis in the testis remains far behind that in other epithelia and tissues. The goal of this review is to bridge this gap.
Search for other papers by Jiarong Feng in
Google Scholar
PubMed
Search for other papers by Yanan Zhang in
Google Scholar
PubMed
Search for other papers by Xiaojian Yang in
Google Scholar
PubMed
Search for other papers by Yan Zhang in
Google Scholar
PubMed
In brief
The genetic heterogeneity of CFTR gene mutations in Chinese patients with congenital absence of the vas deferens (CAVD) differs from the hotspot mutation pattern in Caucasians. This paper reviews and suggests a more suitable screening strategy for the Chinese considering the dilemma of CFTR genetic blocking.
Abstract
Congenital absence of the vas deferens (CAVD) is a major cause of obstructive azoospermia and male infertility, with CFTR gene mutation as the main pathogenesis. Other genes such as ADGRG2, SLC9A3, and PANK2 have been discovered and proven to be associated with CAVD in recent studies. Multiple CFTR hotspot mutations have been found in Caucasians in several foreign countries, and relevant genetic counseling and preimplantation genetic diagnosis (PGD) have been conducted for decades. However, when we examined research on Chinese CAVD, we discovered that CFTR mutations show heterogeneity in the Chinese Han population, and there is currently no well-established screening strategy. Therefore, we have reviewed the literature, combining domestic and international research as well as our own, aiming to review research progress on the CFTR gene in China and discuss the appropriate scope for CFTR gene detection, the detection efficiency of other CAVD-related genes, and the screening strategy applicable to the Chinese Han population. This study provides more valuable information for genetic counseling and a theoretical basis for PGD and treatment for couples with CAVD when seeking reproductive assistance.
Search for other papers by Xiaokui Yang in
Google Scholar
PubMed
Search for other papers by Ying Zhou in
Google Scholar
PubMed
Search for other papers by Sha Peng in
Google Scholar
PubMed
Department of Human Reproductive Medicine, State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing 100006, China
Search for other papers by Liang Wu in
Google Scholar
PubMed
Search for other papers by Hai-Yan Lin in
Google Scholar
PubMed
Search for other papers by Shuyu Wang in
Google Scholar
PubMed
Search for other papers by Hongmei Wang in
Google Scholar
PubMed
Recent studies implicate the regulatory function of microRNAs (miRNAs) in oocyte maturation and ovarian follicular development. Differentially expressed miRNAs are found in the plasma of premature ovarian failure (POF) patients and normal cycling women. In this study, miRNA-regulated signaling pathways and related genes were described using Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis. The effect of mir-23a on granulosa cell apoptosis was also studied by examining the protein expression of X-linked inhibitor of apoptosis protein (XIAP) and caspase-3, followed by subsequent counting of apoptotic cells after Hoechst 33258 staining. Both GO analysis and pathway analysis suggested that many signaling pathways, including the AKT signaling pathway, steroid hormone receptor signaling pathways, and others, were regulated by this group of differentially expressed miRNAs. A decrease in XIAP expression (mRNA and protein level) and caspase-3 protein levels and an increase in cleaved caspase-3 protein were observed in human ovarian granulosa cells transfected with pre-mir-23a, along with an increased occurrence of apoptosis. In conclusion, differentially expressed miRNAs in the plasma of POF patients may have regulatory effects on proliferation and apoptosis of granulosa cells by affecting different signaling pathways. Mir-23a may play important roles in regulating apoptosis via decreasing XIAP expression in human ovarian granulosa cells.
Search for other papers by Nan Meng in
Google Scholar
PubMed
Search for other papers by Xinyue Wang in
Google Scholar
PubMed
Search for other papers by Yan Shi in
Google Scholar
PubMed
Search for other papers by Yanyan Mao in
Google Scholar
PubMed
Search for other papers by Qian Yang in
Google Scholar
PubMed
Search for other papers by Baohui Ju in
Google Scholar
PubMed
Search for other papers by Qianxi Zhu in
Google Scholar
PubMed
Search for other papers by Tingting Zhang in
Google Scholar
PubMed
Search for other papers by Yan Gu in
Google Scholar
PubMed
Search for other papers by Xuan Zhang in
Google Scholar
PubMed
Decidualization is essential for the successful establishment of pregnancy, and the dysregulated decidualization may lead to early pregnancy loss. It was previously reported by us that miR-3074-5p could promote apoptosis but inhibit invasion of human extravillous trophoblast (EVT) cells in vitro, and the expression level of miR-3074-5p in villus tissues of recurrent miscarriage (RM) patients was significantly increased. The aim of this study was to preliminarily explore the role of miR-3074-5p played in the decidualization of human endometrial stromal cells (ESCs). It was found that the decidual expression level of miR-3074-5p in RM patients was remarkably higher than that in the control group. The overexpression of miR-3074-5p in the immortalized human ESC line, T-HESCs, showed suppressive effects not only on the cell proliferation, as well as the intracellular expression levels of cyclin B1 (CCNB1), CCND1 and CCNE1 but also on the in vitro-induced decidualization. CLN8 mRNA, encoding an endoplasmic reticulum (ER)-associated membrane protein, was validated to be directly targeted by miR-3074-5p. And, the expression level of CLN8 was continuously increased along with the decidualization process, whereas down-regulated CLN8 expression could inhibit the decidualization of T-HESCs in vitro. Furthermore, contrary to the increased expression level of miR-3074-5p, a significantly decreased CLN8 expression was observed in decidual tissues of RM patients. Collectively, these data suggested that an increased miR-3074-5p expression in ESCs might cause early pregnancy failure by disturbing decidualization of ESCs via the miR-3074-5p/CLN8 pathway, providing a potential diagnostic and therapeutic target for RM.
College of Life Science, Shandong Normal University, Jinan, People’s Republic of China
Search for other papers by Xiaohui Cui in
Google Scholar
PubMed
Search for other papers by Yan Sun in
Google Scholar
PubMed
Search for other papers by Xiuge Wang in
Google Scholar
PubMed
Search for other papers by Chunhong Yang in
Google Scholar
PubMed
Search for other papers by Zhihua Ju in
Google Scholar
PubMed
Search for other papers by Qiang Jiang in
Google Scholar
PubMed
Search for other papers by Yan Zhang in
Google Scholar
PubMed
Search for other papers by Jinming Huang in
Google Scholar
PubMed
Search for other papers by Jifeng Zhong in
Google Scholar
PubMed
Search for other papers by Miao Yin in
Google Scholar
PubMed
Search for other papers by Changfa Wang in
Google Scholar
PubMed
The micromolar calcium-activated neutral protease gene (CAPN1) is a physiological candidate gene for sperm motility. However, the molecular mechanisms involved in regulating the expression of the CAPN1 gene in bulls remain unknown. In this study, we investigated the expression pattern of CAPN1 in testis, epididymis, and sperm at the RNA and protein levels by qRT-PCR, western blot, immunohistochemistry, and immunofluorescence assay. Results revealed that the expression of CAPN1 levels was higher in the sperm head compared with that in other tissues. Moreover, we identified a novel single-nucleotide polymorphism (g.-1256 A>C, ss 1917715340) in the noncanonical core promoter of the CAPN1 gene between base g.-1306 and g.-1012. Additionally, we observed greater sperm motility in bulls with the genotype CC than in those with the genotype AA (P<0.01), indicating that different genotypes were associated with the bovine semen trait. Furthermore, a higher fluorescence intensity of the C allele than that of the A allele at g. -1256 A>C was revealed by transient transfection in MLTC-1 cells and luciferase report assay. Finally, CAPN1 was highly expressed in the spermatozoa with the CC genotype compared with that with the AA genotype by qRT-PCR. This study is the first report on genetic variant g.-1256 A>C in the promoter region of CAPN1 gene association with the semen quality of Chinese Holstein bulls by influencing its expression. g.-1256 A>C can be a functional molecular marker in cattle breeding.
Search for other papers by Shuai Lin in
Google Scholar
PubMed
Search for other papers by Yu-Yuan Zhu in
Google Scholar
PubMed
Search for other papers by Wei Hu in
Google Scholar
PubMed
Search for other papers by Yan Yang in
Google Scholar
PubMed
Search for other papers by Jia-Mei Luo in
Google Scholar
PubMed
Search for other papers by Shi-Jun Hu in
Google Scholar
PubMed
Search for other papers by Zeng-Ming Yang in
Google Scholar
PubMed
Decidualization is required for the successful establishment of pregnancy in rodents and primates. Fatty acid desaturase 3 (Fads3) belongs to the fatty acid desaturase family, which is a crucial enzyme for highly unsaturated fatty acid biosynthesis. However, the expression, regulation and function of Fads3 during early pregnancy in mice are still unknown. In this study, we examined Fads3 expression, regulation and function during mouse decidualization. The expression of Fads3 is detected in the subluminal stromal cells at implantation site on day 5 of pregnancy, but not at inter-implantation site and in day 5 pseudopregnant uteri. Compared to delayed implantation, Fads3 is strongly expressed after delayed implantation is activated by estrogen treatment. From days 6 to 8, Fads3 mRNA signals are significantly detected in the decidua. In ovariectomized mice, estrogen significantly stimulates Fads3 expression. However, estrogen has no effect on Fads3 expression in ovariectomized ERα-deficient mice, suggesting that estrogen regulation on Fads3 expression is ERα dependent. When ovariectomized mice were treated with progesterone, Fads3 expression is significantly increased by progesterone. Progesterone stimulation on Fads3 expression is also detected in cultured stromal cells, which is abrogated by RU486 treatment. These data indicate that progesterone upregulation on Fads3 expression is progesterone receptor-dependent. Fads3 knockdown by siRNA reduces in vitro decidualization of mouse stromal cells. Taken together, Fads3 may play an important role during mouse decidualization.
Search for other papers by Wen-Wen Gu in
Google Scholar
PubMed
Search for other papers by Long Yang in
Google Scholar
PubMed
Search for other papers by Xing-Xing Zhen in
Google Scholar
PubMed
Search for other papers by Yan Gu in
Google Scholar
PubMed
Search for other papers by Hua Xu in
Google Scholar
PubMed
Search for other papers by Miao Liu in
Google Scholar
PubMed
Search for other papers by Qian Yang in
Google Scholar
PubMed
Search for other papers by Xuan Zhang in
Google Scholar
PubMed
Search for other papers by Jian Wang in
Google Scholar
PubMed
The invasion of maternal decidua by extravillous trophoblast (EVT) is essential for the establishment and maintenance of pregnancy, and abnormal trophoblast invasion could lead to placenta-associated pathologies including early pregnancy loss and preeclampsia. SEC5, a component of the exocyst complex, plays important roles in cell survival and migration, but its role in early pregnancy has not been reported. Thus, the present study was performed to explore the functions of SEC5 in trophoblast cells. The results showed that SEC5 expression in human placental villi at first trimester was significantly higher than it was at the third trimester, and it was abundantly localized in the cytotrophoblast (CTB) and the trophoblastic column. SEC5 knockdown was accompanied by reduced migration and invasion in HTR-8/SVneo cells. In addition, the expression and plasma membrane distribution of integrin β1 was also decreased. Furthermore, shRNA-mediated knockdown of SEC5 inhibited the outgrowth of first trimester placental explants. SEC5 and InsP3R were colocalized in the cytoplasm of HTR-8/SVneo cells, and the cell-permeant calcium chelator BAPTA-AM could significantly inhibit HTR-8/SVneo cell invasion. The Ca2+ imaging results showed that the 10% fetal bovine serum-stimulated cytosolic calcium concentration ([Ca2+]c) was not only reduced by downregulated SEC5 but also was blocked by the InsP3R inhibitor. Furthermore, either the [Ca2+]c was buffered by BAPTA-AM or the knockdown of SEC5 disrupted HTR-8/SVneo cell F-actin stress fibers and caused cytoskeleton derangement. Taken together, our results suggest that SEC5 might be involved in regulating trophoblast cell migration and invasion through the integrin/Ca2+ signal pathway to induce cytoskeletal rearrangement.
College of Veterinary Medicine, South China Agricultural University, Guangzhou, China
Search for other papers by Yu-Xiang Liang in
Google Scholar
PubMed
College of Life Science and Resources and Environment, Yichun University, Yichun, China
Search for other papers by Wei Hu in
Google Scholar
PubMed
Search for other papers by Zhi-Yong Jin in
Google Scholar
PubMed
Search for other papers by Hong-Lu Diao in
Google Scholar
PubMed
Search for other papers by Li Liu in
Google Scholar
PubMed
Search for other papers by Yan Yang in
Google Scholar
PubMed
Search for other papers by Tao Fu in
Google Scholar
PubMed
Search for other papers by Zeng-Ming Yang in
Google Scholar
PubMed
Embryo implantation and decidualization are crucial steps during early pregnancy. We recently showed that nucleolar stress is involved in embryo implantation. This study was to explore whether nucleolar stress participates in mouse and human decidualization. Our data demonstrated that a low dose of actinomycin D (ActD) could induce nucleolar stress in stroma cells. Nucleolar stress promotes the stromal-epithelial transition during mouse in vitro decidualization through nucleophosmin1 (NPM1). Under nucleolar stress, Wnt family member 4 (Wnt4), a decidualization marker, is significantly increased, but decidua/trophoblast prolactin-related protein (Dtprp/Prl8a2) expression remains unchanged. For translational significance, we also examined the effects of nucleolar stress on human decidualization. Nucleolar stress stimulated by a low dose of ActD enhances human stromal–epithelial transition during human decidualization, but has no effects on the expression of insulin-like growth factor-binding protein 1 (IGFBP1). Our study indicates that nucleolar stress may promote only the mesenchymal–epithelial transition (MET), but not for all the molecular changes during decidualization.
Department of Obstetrics and Gynaecology, Key Laboratory of Assisted Reproduction, Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Neuroscience Research Institute, Center for Reproductive Medicine, Peking University Third Hospital, No. 49, North Huayuan Road, Haidian District, Beijing 100191, China
Department of Obstetrics and Gynaecology, Key Laboratory of Assisted Reproduction, Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Neuroscience Research Institute, Center for Reproductive Medicine, Peking University Third Hospital, No. 49, North Huayuan Road, Haidian District, Beijing 100191, China
Search for other papers by Haolin Zhang in
Google Scholar
PubMed
Search for other papers by Ming Yi in
Google Scholar
PubMed
Department of Obstetrics and Gynaecology, Key Laboratory of Assisted Reproduction, Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Neuroscience Research Institute, Center for Reproductive Medicine, Peking University Third Hospital, No. 49, North Huayuan Road, Haidian District, Beijing 100191, China
Search for other papers by Yan Zhang in
Google Scholar
PubMed
Department of Obstetrics and Gynaecology, Key Laboratory of Assisted Reproduction, Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Neuroscience Research Institute, Center for Reproductive Medicine, Peking University Third Hospital, No. 49, North Huayuan Road, Haidian District, Beijing 100191, China
Search for other papers by Hongyan Jin in
Google Scholar
PubMed
Department of Obstetrics and Gynaecology, Key Laboratory of Assisted Reproduction, Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Neuroscience Research Institute, Center for Reproductive Medicine, Peking University Third Hospital, No. 49, North Huayuan Road, Haidian District, Beijing 100191, China
Search for other papers by Wenxin Zhang in
Google Scholar
PubMed
Department of Obstetrics and Gynaecology, Key Laboratory of Assisted Reproduction, Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Neuroscience Research Institute, Center for Reproductive Medicine, Peking University Third Hospital, No. 49, North Huayuan Road, Haidian District, Beijing 100191, China
Search for other papers by Jingjing Yang in
Google Scholar
PubMed
Department of Obstetrics and Gynaecology, Key Laboratory of Assisted Reproduction, Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Neuroscience Research Institute, Center for Reproductive Medicine, Peking University Third Hospital, No. 49, North Huayuan Road, Haidian District, Beijing 100191, China
Search for other papers by Liying Yan in
Google Scholar
PubMed
Department of Obstetrics and Gynaecology, Key Laboratory of Assisted Reproduction, Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Neuroscience Research Institute, Center for Reproductive Medicine, Peking University Third Hospital, No. 49, North Huayuan Road, Haidian District, Beijing 100191, China
Search for other papers by Rong Li in
Google Scholar
PubMed
Department of Obstetrics and Gynaecology, Key Laboratory of Assisted Reproduction, Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Neuroscience Research Institute, Center for Reproductive Medicine, Peking University Third Hospital, No. 49, North Huayuan Road, Haidian District, Beijing 100191, China
Search for other papers by Yue Zhao in
Google Scholar
PubMed
Department of Obstetrics and Gynaecology, Key Laboratory of Assisted Reproduction, Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Neuroscience Research Institute, Center for Reproductive Medicine, Peking University Third Hospital, No. 49, North Huayuan Road, Haidian District, Beijing 100191, China
Department of Obstetrics and Gynaecology, Key Laboratory of Assisted Reproduction, Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Neuroscience Research Institute, Center for Reproductive Medicine, Peking University Third Hospital, No. 49, North Huayuan Road, Haidian District, Beijing 100191, China
Search for other papers by Jie Qiao in
Google Scholar
PubMed
Polycystic ovary syndrome (PCOS) is a complex endocrine and metabolic disorder with unclear etiology and unsatisfactory management. Effects of diets on the phenotype of PCOS were not fully understood. In the present study, we applied 45 and 60% high-fat diets (HFDs) on a rat model of PCOS induced by postnatal DHEA injection. We found that both DHEA and DHEA+HFDs rats exhibited reproductive abnormalities, including hyperandrogenism, irregular cycles and polycystic ovaries. The addition of HFDs, especially 60% HFDs, exaggerated morphological changes of ovaries and a number of metabolic changes, including increased body weight and body fat content, impaired glucose tolerance and increased serum insulin levels. Results from qPCR showed that DHEA-induced increased expression of hypothalamic androgen receptor and LH receptor were reversed by the addition of 60% HFDs. In contrast, the ovarian expression of LH receptor and insulin receptor mRNA was upregulated only with the addition of 60% HFDs. These findings indicated that DHEA and DHEA+HFDs might influence PCOS phenotypes through distinct mechanisms: DHEA affects the normal function of hypothalamus–pituitary–ovarian axis through LH, whereas the addition of HFDs exaggerated endocrine and metabolic dysfunction through ovarian responses to insulin-related mechanisms. We concluded that the addition of HFDs yielded distinct phenotypes of DHEA-induced PCOS and could be used for studies on both reproductive and metabolic features of the syndrome.
Search for other papers by Hua-Yu Lian in
Google Scholar
PubMed
Search for other papers by Yan Gao in
Google Scholar
PubMed
Search for other papers by Guang-Zhong Jiao in
Google Scholar
PubMed
Search for other papers by Ming-Ju Sun in
Google Scholar
PubMed
Search for other papers by Xiu-Fen Wu in
Google Scholar
PubMed
Search for other papers by Tian-Yang Wang in
Google Scholar
PubMed
Search for other papers by Hong Li in
Google Scholar
PubMed
Search for other papers by Jing-He Tan in
Google Scholar
PubMed
In this study, using a mouse model, we tested the hypothesis that restraint stress would impair the developmental potential of oocytes by causing oxidative stress and that antioxidant supplementation could overcome the adverse effect of stress-induced oxidative stress. Female mice were subjected to restraint stress for 24 h starting 24 h after equine chorionic gonadotropin injection. At the end of stress exposure, mice were either killed to recover oocytes for in vitro maturation (IVM) or injected with human chorionic gonadotropin and caged with male mice to observe in vivo development. The effect of antioxidants was tested in vitro by adding them to IVM medium or in vivo by maternal injection immediately before restraint stress exposure. Assays carried out to determine total oxidant and antioxidant status, oxidative stress index, and reactive oxygen species (ROS) and glutathione levels indicated that restraint stress increased oxidative stress in mouse serum, ovaries, and oocytes. Whereas the percentage of blastocysts and number of cells per blastocyst decreased significantly in oocytes from restraint-stressed mice, addition of antioxidants to IVM medium significantly improved their blastocyst development. Supplementation of cystine and cysteamine to IVM medium reduced ROS levels and aneuploidy while increasing glutathione synthesis and improving pre- and postimplantation development of oocytes from restraint-stressed mice. Furthermore, injection of the antioxidant epigallocatechin gallate into restraint-stressed mice significantly improved the blastocyst formation and postimplantation development of their oocytes. In conclusion, restraint stress at the oocyte prematuration stage impaired the developmental potential of oocytes by increasing oxidative stress and addition of antioxidants to IVM medium or maternal antioxidant injection overcame the detrimental effect of stress-induced oxidative stress. The data reported herein are helpful when making attempts to increase the chances of a successful outcome in human IVF, because restraint was applied at a stage similar to the FSH stimulation period in a human IVF program.
