Search Results
You are looking at 1 - 10 of 10 items for
- Author: Jian Zhang x
- Refine by access: All content x
Institute of Embryo-Fetal Original Adult Disease, Affiliated to School of Medicine, Shanghai Jiaotong University, Shanghai, China
Search for other papers by Hang Qi in
Google Scholar
PubMed
Institute of Embryo-Fetal Original Adult Disease, Affiliated to School of Medicine, Shanghai Jiaotong University, Shanghai, China
Search for other papers by Guiling Liang in
Google Scholar
PubMed
Institute of Embryo-Fetal Original Adult Disease, Affiliated to School of Medicine, Shanghai Jiaotong University, Shanghai, China
Search for other papers by Jin Yu in
Google Scholar
PubMed
Institute of Embryo-Fetal Original Adult Disease, Affiliated to School of Medicine, Shanghai Jiaotong University, Shanghai, China
Search for other papers by Xiaofeng Wang in
Google Scholar
PubMed
Institute of Embryo-Fetal Original Adult Disease, Affiliated to School of Medicine, Shanghai Jiaotong University, Shanghai, China
Search for other papers by Yan Liang in
Google Scholar
PubMed
Institute of Embryo-Fetal Original Adult Disease, Affiliated to School of Medicine, Shanghai Jiaotong University, Shanghai, China
Search for other papers by Xiaoqing He in
Google Scholar
PubMed
Search for other papers by Tienan Feng in
Google Scholar
PubMed
Institute of Embryo-Fetal Original Adult Disease, Affiliated to School of Medicine, Shanghai Jiaotong University, Shanghai, China
Search for other papers by Jian Zhang in
Google Scholar
PubMed
MicroRNA (miRNA) expression profiles in tubal endometriosis (EM) are still poorly understood. In this study, we analyzed the differential expression of miRNAs and the related gene networks and signaling pathways in tubal EM. Four tubal epithelium samples from tubal EM patients and five normal tubal epithelium samples from uterine leiomyoma patients were collected for miRNA microarray. Bioinformatics analyses, including Ingenuity Pathway Analysis (IPA), Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, were performed. Quantitative real-time polymerase chain reaction (qRT-PCR) validation of five miRNAs was performed in six tubal epithelium samples from tubal EM and six from control. A total of 17 significantly differentially expressed miRNAs and 4343 potential miRNA-target genes involved in tubal EM were identified (fold change >1.5 and FDR-adjusted P value <0.05). IPA indicated connections between miRNAs, target genes and other gynecological diseases like endometrial carcinoma. GO and KEGG analysis revealed that most of the identified genes were involved in the mTOR signaling pathway, SNARE interactions in vesicular transport and endocytosis. We constructed an miRNA-gene-disease network using target gene prediction. Functional analysis showed that the mTOR pathway was connected closely to tubal EM. Our results demonstrate for the first time the differentially expressed miRNAs and the related signal pathways involved in the pathogenesis of tubal EM which contribute to elucidating the pathogenic mechanism of tubal EM-related infertility.
Search for other papers by Hongzheng Sun in
Google Scholar
PubMed
Search for other papers by Jianmin Su in
Google Scholar
PubMed
Search for other papers by Teng Wu in
Google Scholar
PubMed
Search for other papers by Fengyu Wang in
Google Scholar
PubMed
Search for other papers by Jian Kang in
Google Scholar
PubMed
Search for other papers by Jingcheng Zhang in
Google Scholar
PubMed
Search for other papers by Xupeng Xing in
Google Scholar
PubMed
Search for other papers by Yuyao Cheng in
Google Scholar
PubMed
Search for other papers by Yong Zhang in
Google Scholar
PubMed
Coactivator-associated arginine methyltransferase 1 (CARM1) is a type I arginine methyltransferase that methylates the arginine residues of histone and nonhistone. Carm1 regulates various cellular processes, including transcriptional regulation, mRNA processing, cellular proliferation, and differentiation. Blastomeres with high Carm1 expression levels show cleavage tendency to inner cell mass (ICM) in mouse embryos. However, details about the factors for CARM1 distribution in mouse early embryos and the role of Carm1 in blastocyst development remain unclear. Here, the endonuclear distribution of CARM1 protein was heterogeneous between blastomeres from the late four-cell stage to the blastocyst stage. The heterogeneity of CARM1 distribution in blastomeres at the late four-cell stage was randomly obtained from two-cell stage embryos. From the four-cell stage to morula, CARM1 in individual blastomere remained heterogeneous. In the blastocyst stage, CARM1 protein level in ICM was much higher than that in trophoblast. We found that microRNA (miRNA) miR-181a is an important regulator for Carm1 distribution at the late four-cell stage. The ratio of heterogeneous embryos was reduced in all the embryos when miR-181a was inhibited. CARM1 inhibition reduced the level of symmetrical histone H3 arginine-26 dimethylation and impaired blastocyst development. Silencing Carm1 reduced cell number and increased cell apoptosis at the blastocyst stage. These results show a CARM1 heterogeneous distribution from the four-cell embryos to the blastocysts. miR-181a regulates the control of CARM1 heterogeneous distribution in the four-cell-stage embryos, and CARM1 is an important protein in regulating blastocyst development.
Shanghai Key Laboratory Embryo Original Diseases, Shanghai, China
Search for other papers by Hang Qi in
Google Scholar
PubMed
Shanghai Key Laboratory Embryo Original Diseases, Shanghai, China
Search for other papers by Huiyu Zhang in
Google Scholar
PubMed
Shanghai Key Laboratory Embryo Original Diseases, Shanghai, China
Search for other papers by Xiaoya Zhao in
Google Scholar
PubMed
Search for other papers by Ya Qin in
Google Scholar
PubMed
Shanghai Key Laboratory Embryo Original Diseases, Shanghai, China
Search for other papers by Guiling Liang in
Google Scholar
PubMed
Shanghai Key Laboratory Embryo Original Diseases, Shanghai, China
Search for other papers by Xiaoqing He in
Google Scholar
PubMed
Shanghai Key Laboratory Embryo Original Diseases, Shanghai, China
Search for other papers by Jian Zhang in
Google Scholar
PubMed
Tubal endometriosis (tubal EM) is a subtype of endometriosis (EM) associated with fallopian tube impairments and infertility. Since the molecular mechanism underlying tubal EM is not clear, we assume that an aberrant transcriptome of fallopian tube epithelium and microenvironment changes caused by cytokines in tubal fluid are possible causes. The aim of this study was to identify potential hub mRNAs/proteins of tubal EM through integrated transcriptomic and proteomic analyses and to elucidate significant pathways, cellular functions, and interaction networks during the initiation and progression of tubal EM. We obtained human fallopian tube epithelium and tubal fluid samples from patients with and without tubal EM. Tubal epithelia were analyzed using microarray, and tubal fluid was analyzed using quantitative label-free LC-MS/MS. We identified differentially expressed genes (DEGs) and differentially expressed proteins (DEPs) and determined common mRNAs/protein. We observed 35 commonly deregulated mRNAs/proteins, and IPA indicated that cellular movement, inflammatory response, and immune cell trafficking were significantly activated during the pathogenesis of tubal EM. We also identified acute phase response signaling pathway activation as a unique pathogenesis signature of tubal EM. Our results demonstrate that an integrated analysis of the transcriptome and proteome has the potential to reveal novel disease mechanisms at a molecular level.
Department of Biology, Southern University of Science and Technology, Shenzhen, Guangdong, China
Search for other papers by Jian Zhang in
Google Scholar
PubMed
Search for other papers by Linlin Hao in
Google Scholar
PubMed
Search for other papers by Qian Wei in
Google Scholar
PubMed
Search for other papers by Sheng Zhang in
Google Scholar
PubMed
Search for other papers by Hui Cheng in
Google Scholar
PubMed
Search for other papers by Yanhui Zhai in
Google Scholar
PubMed
Search for other papers by Yu Jiang in
Google Scholar
PubMed
Search for other papers by Xinglan An in
Google Scholar
PubMed
Search for other papers by Ziyi Li in
Google Scholar
PubMed
Search for other papers by Xueming Zhang in
Google Scholar
PubMed
Search for other papers by Bo Tang in
Google Scholar
PubMed
Somatic cell nuclear transfer (SCNT) has been successfully used for cloning in a variety of mammalian species. However, SCNT reprogramming efficiency is relatively low, in part, due to incomplete DNA methylation reprogramming of donor cell nuclei. We previously showed that ten-eleven translocation 3 (TET3) is responsible for active DNA demethylation during preimplantation embryonic development in bovines. In this study, we constructed TET3-overexpressing cell lines in vitro and observed that the use of these fibroblasts as donor cells increased the blastocyst rate by approximately 18 percentage points compared to SCNT. The overexpression of TET3 in bovine SCNT embryos caused a decrease in the global DNA methylation level of the pluripotency genes Nanog and Oct-4, ultimately resulting in an increase in the transcriptional activity of these pluripotency genes. Moreover, the quality of bovine TET3-NT embryos at the blastocyst stage was significantly improved, and bovine TET3-NT blastocysts possessed more total number of cells and fewer apoptotic cells than the SCNT blastocysts, similar to in vitro fertilization (IVF) embryos. Nevertheless, DNA methylation of the imprinting control region (ICR) for the imprinted genes H19-IGF2 in SCNT embryos remained unaffected by TET3 overexpression, maintaining parent-specific activity for further development. Thus, the results of our study provide a promising approach to rectify incomplete epigenetic reprogramming and achieve higher cloning efficiency.
Search for other papers by Zi-gang Shen in
Google Scholar
PubMed
Search for other papers by Wei He in
Google Scholar
PubMed
Search for other papers by Ji Zhang in
Google Scholar
PubMed
Search for other papers by Hai-yang He in
Google Scholar
PubMed
Search for other papers by Xia Yang in
Google Scholar
PubMed
Search for other papers by Zheng-qiong Chen in
Google Scholar
PubMed
Search for other papers by Ping Yang in
Google Scholar
PubMed
Search for other papers by Jian Li in
Google Scholar
PubMed
Search for other papers by Zhi-qing Liang in
Google Scholar
PubMed
Search for other papers by Yu-zhang Wu in
Google Scholar
PubMed
Search for other papers by Jin-tao Li in
Google Scholar
PubMed
SPINLW1 (previously known as eppin (epididymal protease inhibitor)) is a target under intense scrutiny in the study of male contraceptive vaccines. B-cell-dominant epitopes are now recognized as key parts of the induction of humoral immune responses against target antigens. The generation of robust humoral responses in vivo has become a crucial problem in the development of modern vaccines. In this study, we developed a completely novel B-cell-dominant-epitope-based mimovirus vaccine, which is a kind of virus-size particulate antigen delivery system. The mimovirus successfully self-assembled from a cationic peptide containing a cell-penetrating peptide of TAT49–57 and a plasmid DNA encoding both three SPINLW1 (103–115) copies and adjuvant C3d3. The male mice were immunized with the epitope-based mimovirus vaccine, which resulted in a gradual elevation of specific serum IgG antibody levels. These reached a peak at week 4. Mating for the fertility assay showed that the mimovirus vaccine had accomplished a moderate fertility inhibition effect and investigation into the mechanism of action showed that it did so by interfering with the reproductive function of the sperm but that it did not damage the structures of the testes or cause serum testosterone to decline. Our results suggest an ideal protocol for suppressing fertility in mice by an engineered mimovirus vaccine.
College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Yufei Wang in
Google Scholar
PubMed
College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Haoya Chang in
Google Scholar
PubMed
College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Qifu He in
Google Scholar
PubMed
College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Yaxing Xue in
Google Scholar
PubMed
College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Kang Zhang in
Google Scholar
PubMed
College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Jian Kang in
Google Scholar
PubMed
College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Ying Wang in
Google Scholar
PubMed
College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Zhiming Xu in
Google Scholar
PubMed
College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Yong Zhang in
Google Scholar
PubMed
College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China
Search for other papers by Fusheng Quan in
Google Scholar
PubMed
Oocyte vitrification has significantly improved the survival rate and become the mainstream method for cryopreserving oocytes. Previous studies have demonstrated that the ultrastructure, mitochondrial function, DNA methylation, and histone modification exhibit an irreversible effect after oocyte vitrification. However, little is known about the effects of oocyte vitrification on glucose transport and metabolism. This study aims to determine whether mouse oocyte vitrification causes abnormal glucose metabolism and identify a strategy to correct abnormal glucose metabolism. Furthermore, this study further investigates the effects of oocyte vitrification on glucose uptake, and glucose metabolism, and energy levels. The results indicated that vitrification significantly reduced the glucose transport activity, NADPH, glutathione, and ATP levels, and increased reactive oxygen species levels in oocytes (P < 0.01). Vitrification also reduced the expression of glucose transporter isoform 1 (GLUT1) (P < 0.01). Adding a GLUT1 inhibitor reduced the glucose uptake capacity of oocytes. Furthermore, the inclusion of vitamin C into thawing and culture solutions restored abnormal glucose transportation and metabolism and improved the survival, two-cell embryo, and blastocyst rates of the vitrified groups via parthenogenesis (P < 0.05). Overall, this method may improve the quality and efficiency of oocyte vitrification.
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.
Search for other papers by Kang Zhang in
Google Scholar
PubMed
Search for other papers by Tianyang Lan in
Google Scholar
PubMed
Search for other papers by Feifei Lin in
Google Scholar
PubMed
Search for other papers by Ruichuan Liu in
Google Scholar
PubMed
Search for other papers by Qifu He in
Google Scholar
PubMed
Search for other papers by Feng Gao in
Google Scholar
PubMed
Search for other papers by Shenghui Wu in
Google Scholar
PubMed
Search for other papers by Jian Kang in
Google Scholar
PubMed
Search for other papers by Hongmin Li in
Google Scholar
PubMed
Search for other papers by Fusheng Quan in
Google Scholar
PubMed
In brief
Oocyte vitrification leads to DNA hypomethylation, which results in defect in early embryo development. This study reveals that oocyte vitrification impairs the DNA methylation pattern by influencing protein O-GlcNAcylation.
Abstract
Oocyte vitrification leads to decreased DNA methylation levels, which impairs the quality and the developmental potential of oocytes. However, the underlying molecular mechanism still need to be further revealed. In this study, mouse metaphase II (M II) oocytes were frozen by vitrification technology, while fresh oocytes were used as the control group. The effect of oocyte vitrification on protein O-GlcNAcylation and its impact on the developmental potential of oocytes were elucidated. We found that the protein O-GlcNAcylation levels were significantly increased in vitrified oocytes. Increase of protein O-GlcNAcylation levels in control oocytes by PUGNAc (an O-GlcNAcase inhibitor) decreases blastocyst rate after parthenogenetic activation (20.82% in PUGNAc-treated group; 53.82% in control group, P < 0.05). We also discovered that DNA methylation was disrupted in two-cell embryos derived from vitrified oocytes, resulting in decreased 5mC and increased 5hmC, showing similar phenotypes to that derived from PUGNAc-treated oocytes. In vitrified and PUGNAc-treated oocytes, O-GlcNAcylated TET3 was significantly increased. Notably, by inhibiting protein O-GlcNAcylation in vitrified oocytes using OSMI1 (an O-GlcNAc transferase inhibitor) we restored the DNA methylation in two-cell embryos and ameliorated the developmental defects in early embryo. Thus, elevated protein O-GlcNAcylation in vitrified oocytes is an essential contributor to their declining embryonic developmental potential. Modulation of protein O-GlcNAcylation improves the developmental potential of vitrified oocytes.
University of Chinese Academy of Sciences, Beijing, China
Search for other papers by Cheng Jin in
Google Scholar
PubMed
Changsha Reproductive Medicine Hospital, Changsha, China
Search for other papers by Yan Zhang in
Google Scholar
PubMed
University of Chinese Academy of Sciences, Beijing, China
Search for other papers by Zhi-Peng Wang in
Google Scholar
PubMed
Search for other papers by Xiu-Xia Wang in
Google Scholar
PubMed
University of Chinese Academy of Sciences, Beijing, China
Search for other papers by Tie-Cheng Sun in
Google Scholar
PubMed
University of Chinese Academy of Sciences, Beijing, China
Search for other papers by Xiao-Yu Li in
Google Scholar
PubMed
University of Chinese Academy of Sciences, Beijing, China
Search for other papers by Ji-Xin Tang in
Google Scholar
PubMed
University of Chinese Academy of Sciences, Beijing, China
Search for other papers by Jin-Mei Cheng in
Google Scholar
PubMed
University of Chinese Academy of Sciences, Beijing, China
Search for other papers by Jian Li in
Google Scholar
PubMed
Search for other papers by Su-Ren Chen in
Google Scholar
PubMed
Search for other papers by Shou-Long Deng in
Google Scholar
PubMed
Search for other papers by Yi-Xun Liu in
Google Scholar
PubMed
Spermatogenesis is crucial for male fertility and is therefore tightly controlled by a variety of epigenetic regulators. However, the function of enhancer of zeste homolog 2 (EZH2) in spermatogenesis and the molecular mechanisms underlying its activity remain poorly defined. Here, we demonstrate that deleting EZH2 promoted spermatogonial differentiation and apoptosis. EZH2 is expressed in spermatogonia, spermatocytes and round and elongated spermatids from stage 9 to 11 but not in leptotene and zygotene spermatocytes. Knocking down Ezh2 in vitro using a lentivirus impaired self-renewal in spermatogonial stem cells (SSCs), and the conditional knockout of Ezh2 in spermatogonial progenitors promoted precocious spermatogonial differentiation. EZH2 functions to balance self-renewal and differentiation in spermatogonia by suppressing NEUROG3 and KIT via a direct interaction that is independent of its histone methyltransferase activity. Moreover, deleting Ezh2 enhanced the activation of CASP3 in spermatids, resulting in reduced spermatozoa production. Collectively, these data demonstrate that EZH2 plays a nonclassical role in the regulation of spermatogonial differentiation and apoptosis in murine spermatogenesis.
Search for other papers by Xue-Ying Zhang in
Google Scholar
PubMed
Search for other papers by Yi-Meng Xiong in
Google Scholar
PubMed
Search for other papers by Ya-Jing Tan in
Google Scholar
PubMed
Search for other papers by Li Wang in
Google Scholar
PubMed
Search for other papers by Rong Li in
Google Scholar
PubMed
Search for other papers by Yong Zhang in
Google Scholar
PubMed
Search for other papers by Xin-Mei Liu in
Google Scholar
PubMed
Search for other papers by Xian-Hua Lin in
Google Scholar
PubMed
Search for other papers by Li Jin in
Google Scholar
PubMed
Search for other papers by Yu-Ting Hu in
Google Scholar
PubMed
Search for other papers by Zhen-Hua Tang in
Google Scholar
PubMed
Search for other papers by Zheng-Mu Wu in
Google Scholar
PubMed
Search for other papers by Feng-Hua Yin in
Google Scholar
PubMed
Search for other papers by Zheng-Quan Wang in
Google Scholar
PubMed
Search for other papers by Ye Xiao in
Google Scholar
PubMed
Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China
Search for other papers by Jian-Zhong Sheng in
Google Scholar
PubMed
The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
Shanghai Key Laboratory of Embryo Original Diseases, Shanghai, China
Search for other papers by He-Feng Huang in
Google Scholar
PubMed
Fertilization failure often occurs during in vitro fertilization (IVF) cycles despite apparently normal sperm and oocytes. Accumulating evidence suggests that mitochondria play crucial roles in the regulation of sperm function and male fertility. 3-Nitrophthalic acid (3-NPA) can induce oxidative stress in mitochondria, and melatonin, as an antioxidant, can improve mitochondrial function by reducing mitochondrial oxidative stress. The role of sperm mitochondrial dysfunction in fertilization failure during IVF is unclear. The present study revealed that spermatozoa with low, or poor, fertilization rates had swollen mitochondria, increased mitochondria-derived ROS, and attenuated mitochondrial respiratory capacity. 3-NPA treatment enhanced mitochondrial dysfunction in sperm. Spermatozoa with poor fertilization rates, and spermatozoa treated with 3-NPA, had reduced penetration ability. The concentration of melatonin was decreased in semen samples with low and poor fertilization rates. Melatonin, not only decreased excessive mitochondria-derived ROS, but also ‘rescued’ the reduced penetration capacity of spermatozoa treated with 3-NPA. Taken together, the study suggested that mitochondria-derived ROS and mitochondrial respiratory capacity are independent bio-markers for sperm dysfunction, and melatonin may be useful in improving sperm quality and overall male fertility.
