Search Results
You are looking at 1 - 9 of 9 items for
- Author: Rui Zhang x
- Refine by access: All content x
Search for other papers by Ruizhi Deng in
Google Scholar
PubMed
Search for other papers by Chengquan Han in
Google Scholar
PubMed
Search for other papers by Lu Zhao in
Google Scholar
PubMed
Search for other papers by Qing Zhang in
Google Scholar
PubMed
Search for other papers by Beifen Yan in
Google Scholar
PubMed
Search for other papers by Rui Cheng in
Google Scholar
PubMed
Search for other papers by Biao Wei in
Google Scholar
PubMed
Search for other papers by Peng Meng in
Google Scholar
PubMed
Search for other papers by Tingchao Mao in
Google Scholar
PubMed
Search for other papers by Yong Zhang in
Google Scholar
PubMed
Search for other papers by Jun Liu in
Google Scholar
PubMed
Endogenous retroviruses (ERVs), which are abundant in mammalian genomes, can modulate the expression of nearby genes, and their expression is dynamic and stage-specific during early embryonic development in mice and humans. However, the functions and mechanisms of ERV elements in regulating embryonic development remain unclear. Here, we utilized several methods to determine the contribution of ERVs to the makeup and regulation of transcripts during embryonic genome activation (EGA). We constructed an ERV library and embryo RNA-seq library (IVF_2c and IVF_8c) of goat to serve as our research basis. The GO and KEGG analysis of nearby ERV genes revealed that some ERV elements may be associated with embryonic development. RNA-seq results were consistent with the features of EGA. To obtain the transcripts derived from the ERV sequences, we blasted the ERV sequences with embryonic transcripts and identified three lncRNAs and one mRNA that were highly expressed in IVF-8c rather than in IVF-2c (q-value <0.05). Then, we validated the expression patterns of nine ERV-related transcripts during early developmental stages and knocked down three high-expression transcripts in EGA. The knockdown of lncRNA TCONS_00460156 or mRNA HSD17B11 significantly decreased the developmental rate of IVF embryos. Our findings suggested that some transcripts from ERVs are essential for the early embryonic development of goat, and analyzing the ERV expression profile during goat EGA may help elucidate the molecular mechanisms of ERV in regulating embryonic development.
Search for other papers by Xu Tengteng in
Google Scholar
PubMed
Search for other papers by Min Gao in
Google Scholar
PubMed
Search for other papers by Ling Zhang in
Google Scholar
PubMed
Search for other papers by Tianqi Cao in
Google Scholar
PubMed
Search for other papers by Yanling Qiu in
Google Scholar
PubMed
Search for other papers by Simiao Liu in
Google Scholar
PubMed
Search for other papers by Wenlian Wu in
Google Scholar
PubMed
Search for other papers by Yitong Zhou in
Google Scholar
PubMed
Search for other papers by Haiying Liu in
Google Scholar
PubMed
Search for other papers by Rui Zhang in
Google Scholar
PubMed
Search for other papers by Xiaohong Ruan in
Google Scholar
PubMed
Search for other papers by Junjiu Huang in
Google Scholar
PubMed
Biallelic variants in the NSUN2 gene cause a rare intellectual disability and female infertility in humans. However, the function and mechanism of NSUN2 during mouse oocyte meiotic maturation and early embryonic development are unknown. Here, we show that NSUN2 is important for mouse oocyte meiotic maturation and early embryonic development. Specifically, NSUN2 is required for ovarian development and oocyte meiosis, and deletion of Nsun2 reduces oocyte maturation and increases the rates of misaligned chromosomes and aberrant spindles. In addition, Nsun2 deficiency results in a low blastocyst rate and impaired blastocyst quality. Strikingly, loss of Nsun2 leads to approximately 35% of embryos being blocked at the 2-cell stage, and Nsun2 knockdown impairs zygotic genome activation at the 2-cell stage. Taken together, these findings suggest that NSUN2 plays a critical role in mouse oocyte meiotic maturation and early embryonic development, and provide key resources for elucidating female infertility with NSUN2 mutations.
Search for other papers by Huan Zhang in
Google Scholar
PubMed
Search for other papers by Xiaohua Jiang in
Google Scholar
PubMed
Search for other papers by Yuanwei Zhang in
Google Scholar
PubMed
Search for other papers by Bo Xu in
Google Scholar
PubMed
Search for other papers by Juan Hua in
Google Scholar
PubMed
Search for other papers by Tieliang Ma in
Google Scholar
PubMed
Search for other papers by Wei Zheng in
Google Scholar
PubMed
Search for other papers by Rui Sun in
Google Scholar
PubMed
Search for other papers by Wei Shen in
Google Scholar
PubMed
Hefei National Laboratory for Physical Sciences at Microscale, Laboratory of Germ Cell Biology, MRC Human Genetics Unit, Department of Obstetrics and Gynecology, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, People's Republic of China
Search for other papers by Howard J Cooke in
Google Scholar
PubMed
Search for other papers by Qiaomei Hao in
Google Scholar
PubMed
Search for other papers by Jie Qiao in
Google Scholar
PubMed
Search for other papers by Qinghua Shi in
Google Scholar
PubMed
In mammals, the primordial follicle pool, providing all oocytes available to a female throughout her reproductive life, is established perinatally. Dysregulation of primordial follicle assembly results in female reproductive diseases, such as premature ovarian insufficiency and infertility. Female mice lacking Dicer1 (Dicer), a gene required for biogenesis of microRNAs, show abnormal morphology of follicles and infertility. However, the contribution of individual microRNAs to primordial follicle assembly remains largely unknown. Here, we report that microRNA 376a (miR-376a) regulates primordial follicle assembly by modulating the expression of proliferating cell nuclear antigen (Pcna), a gene we previously reported to regulate primordial follicle assembly by regulating oocyte apoptosis in mouse ovaries. miR-376a was shown to be negatively correlated with Pcna mRNA expression in fetal and neonatal mouse ovaries and to directly bind to Pcna mRNA 3′ untranslated region. Cultured 18.5 days postcoitum mouse ovaries transfected with miR-376a exhibited decreased Pcna expression both in protein and mRNA levels. Moreover, miR-376a overexpression significantly increased primordial follicles and reduced apoptosis of oocytes, which was very similar to those in ovaries co-transfected with miR-376a and siRNAs targeting Pcna. Taken together, our results demonstrate that miR-376a regulates primordial follicle assembly by modulating the expression of Pcna. To our knowledge, this is the first microRNA–target mRNA pair that has been reported to regulate mammalian primordial follicle assembly and further our understanding of the regulation of primordial follicle assembly.
Search for other papers by Tao Yu in
Google Scholar
PubMed
Search for other papers by Shuai Lin in
Google Scholar
PubMed
Search for other papers by Rui Xu in
Google Scholar
PubMed
Search for other papers by Tian-Xi Du in
Google Scholar
PubMed
Search for other papers by Yang Li in
Google Scholar
PubMed
Search for other papers by Hui Gao in
Google Scholar
PubMed
Search for other papers by Hong-Lu Diao in
Google Scholar
PubMed
Search for other papers by Xiu-Hong Zhang in
Google Scholar
PubMed
Embryo implantation is a crucial step for the successful establishment of mammalian pregnancy. Cyclophilin A (CYPA) is a ubiquitously expressed intracellular protein and is secreted in response to inflammatory stimuli to regulate diverse cellular functions. However, there are currently no reports about the role of CYPA in embryo implantation. Here, we examine the expression pattern of CYPA during mouse early pregnancy and explore the potential role of CYPA during implantation. CYPA is expressed in the subluminal stroma surrounding the implanting blastocyst on day 5 of pregnancy, but not at inter-implantation sites. In ovariectomized mice, estrogen and progesterone significantly stimulate CYPA expression. When pregnant mice are injected intraperitoneally with CYPA inhibitor, the numbers of implantation sites are significantly reduced. Using an in vitro stromal cell culture system, Ppia siRNA knockdown of CYPA and CYPA-specific inhibitor treatment partially inhibits levels of CD147, MMP3 and MMP9. Decreased CYPA expression also significantly inhibits Stat3 activity and expands estrogen responsiveness. Taken together, CYPA may play an important role during mouse embryo implantation.
Key Laboratory of Animal Biotechnology, Ministry of Agriculture and Rural Affairs, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Yanni Jia in
Google Scholar
PubMed
Key Laboratory of Animal Biotechnology, Ministry of Agriculture and Rural Affairs, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Rui Cai in
Google Scholar
PubMed
Key Laboratory of Animal Biotechnology, Ministry of Agriculture and Rural Affairs, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Tong Yu in
Google Scholar
PubMed
Key Laboratory of Animal Biotechnology, Ministry of Agriculture and Rural Affairs, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Ruixue Zhang in
Google Scholar
PubMed
Key Laboratory of Animal Biotechnology, Ministry of Agriculture and Rural Affairs, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Shouqin Liu in
Google Scholar
PubMed
Key Laboratory of Animal Biotechnology, Ministry of Agriculture and Rural Affairs, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by XinYan Guo in
Google Scholar
PubMed
Key Laboratory of Animal Biotechnology, Ministry of Agriculture and Rural Affairs, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Chunmei Shang in
Google Scholar
PubMed
Key Laboratory of Animal Biotechnology, Ministry of Agriculture and Rural Affairs, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Aihua Wang in
Google Scholar
PubMed
Key Laboratory of Animal Biotechnology, Ministry of Agriculture and Rural Affairs, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Yaping Jin in
Google Scholar
PubMed
Key Laboratory of Animal Biotechnology, Ministry of Agriculture and Rural Affairs, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Pengfei Lin in
Google Scholar
PubMed
Decidualization is a critical process for successful embryo implantation and subsequent placenta formation. The characterization and physiological function of lncRNA during decidualization remain largely unknown. In the present study, we conducted RNA-sequencing analysis to compare gene expression between decidua of days 6 and 8, and normal pregnant endometrium (day 4). A total of 2332 high-confidence putative lncRNA transcripts were expressed. Functional clustering analysis of cis and trans lncRNA targets showed that differentially expressed lncRNAs may regulate multiple gene ontology terms and pathways that have important functions in decidualization. Subsequent analyses using qRT-PCR validated that eight of all lncRNAs were differentially regulated in mice uteri during decidualization, both in vivo and in vitro. Furthermore, we showed that differentially expressed lncRNA of Hand2os1 was specifically detected in stromal cells on days 2 to 5 of pregnancy and was strongly upregulated in decidual cells on days 6–8 of pregnancy. Similarly, Hand2os1 expression was also strongly expressed in decidualized cells following artificial decidualization, both in vivo and in vitro. In uterine stromal cells, P4 was able to significantly upregulate the expression of Hand2os1, but upregulation was impeded by RU486, whereas E2 appeared to have no regulating effect on Hand2os1 expression. Concurrently, Hand2os1 significantly promoted the decidual process in vitro and dramatically increased decidualization markers Prl8a2 and Prl3c1. Our results provide a valuable catalog for better understanding of the functional roles of lncRNAs in pregnant mouse uteri, as it relates to decidualization.
Search for other papers by Min Zhang in
Google Scholar
PubMed
Search for other papers by Jia-Shun Wu in
Google Scholar
PubMed
Search for other papers by Xiao Han in
Google Scholar
PubMed
Search for other papers by Rui-Jie Ma in
Google Scholar
PubMed
Search for other papers by Jia-Li Xu in
Google Scholar
PubMed
Search for other papers by Ming-Tao Xu in
Google Scholar
PubMed
Search for other papers by Hong-Jie Yuan in
Google Scholar
PubMed
Search for other papers by Ming-Jiu Luo in
Google Scholar
PubMed
Search for other papers by Jing-He Tan in
Google Scholar
PubMed
In brief
Genes expressed in cumulus cells might be used as markers for competent oocytes/embryos. This study identified and validated a new group of cumulus expansion and/or apoptosis-regulating genes, which may be used for selection of quality oocytes/embryos.
Abstract
Studies on the mechanisms behind cumulus expansion and cumulus cell (CC) apoptosis are essential for understanding the mechanisms for oocyte maturation. Genes expressed in CCs might be used as markers for competent oocytes and/or embryos. In this study, both in vitro (IVT) and in vivo (IVO) mouse oocyte models with significant difference in cumulus expansion and CC apoptosis were used to identify and validate new genes regulating cumulus expansion and CC apoptosis of mouse oocytes. We first performed mRNA sequencing and bioinformatic analysis using the IVT oocyte model to identify candidate genes. We then analyzed functions of the candidate genes by RNAi or gene overexpression to select the candidate cumulus expansion and CC apoptosis-regulating genes. Finally, we validated the cumulus expansion and CC apoptosis-regulating genes using the IVO oocyte model. The results showed that while Spp1, Sdc1, Ldlr, Ezr and Mmp2 promoted, Bmp2, Angpt2, Edn1, Itgb8, Cxcl10 and Agt inhibited cumulus expansion. Furthermore, Spp1, Sdc1 and Ldlr inhibited CC apoptosis. In conclusion, by using both IVT and IVO oocyte models, we have identified and validated a new group of cumulus expansion and/or apoptosis-regulating genes, which may be used for selection of quality oocytes/embryos and for elucidating the molecular mechanisms behind oocyte maturation.
Department of Obstetrics and Gynecology, Characteristic Medical Center of PAP, Tianjin, People’s Republic of China
Search for other papers by Hai-Yan Hou in
Google Scholar
PubMed
Search for other papers by Xi Wang in
Google Scholar
PubMed
Search for other papers by Qi Yu in
Google Scholar
PubMed
Search for other papers by Hong-Yi Li in
Google Scholar
PubMed
Search for other papers by Shao-Jie Li in
Google Scholar
PubMed
Search for other papers by Rui-Yi Tang in
Google Scholar
PubMed
Search for other papers by Zai-Xin Guo in
Google Scholar
PubMed
Search for other papers by Ya-Qiong Chen in
Google Scholar
PubMed
Search for other papers by Chun-Xiu Hu in
Google Scholar
PubMed
Search for other papers by Zhi-Juan Yang in
Google Scholar
PubMed
Search for other papers by Wen-ke Zhang in
Google Scholar
PubMed
Search for other papers by Yan Qin in
Google Scholar
PubMed
Decline in successful conception decreases more rapidly after 38 years of age owing to follicular depletion and decreased oocyte quality. However, limited information is available regarding the underlying mechanism and the useful treatment. This study aimed to evaluate the effects of growth hormone supplementation on oocyte maturation in vivo in aged and young mice and to determine its effect on mitochondrial function. The influence of three different doses of recombinant human growth hormone (rhGH) (0.4, 0.8 and 1.6 mg/kg/day) for 8 weeks before ovarian stimulation was analyzed. Superovulated oocytes were released from the oviduct of 12-week-old and 40-week-old female C57BL/6J mice 14–16 h after administration of human chorionic gonadotropin. Ovarian follicle and morphological analysis and oocyte maturation parameters were then evaluated. This study is the first, to our knowledge, to report that medium- and high-dose rhGH significantly increases antral follicles in aged mice but anti-Müllerian hormone (AMH) levels. Furthermore, derived oocytes, MII-stage oocyte rate, ATP levels, mitochondrial membrane potential and frequencies of homogeneous mitochondrial distribution increased. In contrast, in both aged and young mice, the mtDNA copy numbers per oocyte were similar before rhGH administration, and upon saline administration, they did not differ significantly. We conclude that medium-dose rhGH supplementation before standard ovarian stimulation regimens improves oocyte quality in aged mice, probably by enhancing mitochondrial functionality.
Search for other papers by Rui-Song Ye in
Google Scholar
PubMed
Search for other papers by Meng Li in
Google Scholar
PubMed
Search for other papers by Chao-Yun Li in
Google Scholar
PubMed
Search for other papers by Qi-En Qi in
Google Scholar
PubMed
Search for other papers by Ting Chen in
Google Scholar
PubMed
Search for other papers by Xiao Cheng in
Google Scholar
PubMed
Search for other papers by Song-Bo Wang in
Google Scholar
PubMed
Search for other papers by Gang Shu in
Google Scholar
PubMed
Search for other papers by Li-Na Wang in
Google Scholar
PubMed
Search for other papers by Xiao-Tong Zhu in
Google Scholar
PubMed
Search for other papers by Qing-Yan Jiang in
Google Scholar
PubMed
Search for other papers by Qian-Yun Xi in
Google Scholar
PubMed
Search for other papers by Yong-Liang Zhang in
Google Scholar
PubMed
FSH plays an essential role in processes involved in human reproduction, including spermatogenesis and the ovarian cycle. While the transcriptional regulatory mechanisms underlying its synthesis and secretion have been extensively studied, little is known about its posttranscriptional regulation. A bioinformatics analysis from our group indicated that a microRNA (miRNA; miR-361-3p) could regulate FSH secretion by potentially targeting the FSHB subunit. Herein, we sought to confirm these findings by investigating the miR-361-3p-mediated regulation of FSH production in primary pig anterior pituitary cells. Gonadotropin-releasing hormone (GnRH) treatment resulted in an increase in FSHB synthesis at both the mRNA, protein/hormone level, along with a significant decrease in miR-361-3p and its precursor (pre-miR-361) levels in time- and dose-dependent manner. Using the Dual-Luciferase Assay, we confirmed that miR-361-3p directly targets FSHB. Additionally, overexpression of miR-361-3p using mimics significantly decreased the FSHB production at both the mRNA and protein levels, with a reduction in both protein synthesis and secretion. Conversely, both synthesis and secretion were significantly increased following miR-361-3p blockade. To confirm that miR-361-3p targets FSHB, we designed FSH-targeted siRNAs, and co-transfected anterior pituitary cells with both the siRNA and miR-361-3p inhibitors. Our results indicated that the siRNA blocked the miR-361-3p inhibitor-mediated upregulation of FSH, while no significant effect on non-target expression. Taken together, our results demonstrate that miR-361-3p negatively regulates FSH synthesis and secretion by targeting FSHB, which provides more functional evidence that a miRNA is involved in the direct regulation of FSH.
Search for other papers by Qing Li in
Google Scholar
PubMed
Search for other papers by Juncen Guo in
Google Scholar
PubMed
Search for other papers by Gelin Huang in
Google Scholar
PubMed
Search for other papers by Nan Wu in
Google Scholar
PubMed
Search for other papers by Su Chen in
Google Scholar
PubMed
Search for other papers by Jing Dai in
Google Scholar
PubMed
Search for other papers by Xueguang Zhang in
Google Scholar
PubMed
Search for other papers by Guohui Zhang in
Google Scholar
PubMed
Search for other papers by Weiwei Zhi in
Google Scholar
PubMed
Search for other papers by Jierui Yan in
Google Scholar
PubMed
Search for other papers by Rui Zheng in
Google Scholar
PubMed
Search for other papers by Fei Yan in
Google Scholar
PubMed
Search for other papers by Zheng Yan in
Google Scholar
PubMed
Search for other papers by Ling Wu in
Google Scholar
PubMed
Search for other papers by Sixian Wu in
Google Scholar
PubMed
Search for other papers by Zhiliang Ji in
Google Scholar
PubMed
Search for other papers by Jiuzhi Zeng in
Google Scholar
PubMed
Search for other papers by Ge Lin in
Google Scholar
PubMed
Search for other papers by Bin Li in
Google Scholar
PubMed
Search for other papers by Wenming Xu in
Google Scholar
PubMed
In brief
PLCZ1 mutations are related to total fertilisation failure (TFF) after intracytoplasmic sperm injection (ICSI), characterised by abnormal oocyte oscillations. The novel PLCZ1 compound heterozygous mutations reported by this study were associated with TFF after ICSI, with one of the mutations indicating a gene dosage effect.
Abstract
Oocyte activation failure is thought to be one of the main factors for total fertilisation failure (TFF) after intracytoplasmic sperm injection (ICSI), which could be induced by abnormal calcium oscillations. Phospholipase C zeta (PLCZ), a sperm factor, is associated with Ca2+ oscillations in mammalian oocytes. To date, some mutations in PLCZ1 (the gene that encodes PLCZ) have been linked to TFF, as demonstrated by the observed reduction in protein levels or activity to induce Ca2+ oscillations. In this study, normozoospermic males whose sperms exhibited TFF after ICSI and their families were recruited. First, mutations in the PLCZ1 sequence were identified by whole exome sequencing and validated using Sanger sequencing. Then, the locations of PLCZ1/PLCZ and the transcript and protein levels in the sperm of the patients were studied. Subsequently, in vitro function analysis and in silico analysis were performed to investigate the function–structure correlation of mutations identified in PLCZ1 using western blotting, immunofluorescence, RT-qPCR, and molecular simulation. Ca2+ oscillations were detected after cRNA microinjection into MII mouse oocytes to investigate calcium oscillations induced by abnormal PLCZ. Five variants with compound heterozygosity were identified, consisting of five new mutations and three previously reported mutations distributed across the main domains of PLCZ, except the EF hands domain. The transcript and protein levels decreased to varying degrees among all detected mutations in PLCZ1 when transfected in HEK293T cells. Among these, mutations in M138V and R391* of PLCZ were unable to trigger typical Ca2+ oscillations. In case 5, aberrant localisation of PLCZ in the sperm head and an increased expression of PLCZ in the sperm were observed. In conclusion, this study enhances the potential for genetic diagnosis of TFF in clinics and elucidates the possible relationship between the function and structure of PLCZ in novel mutations.
