Maternal and Child Health Hospital of Hubei Province

Wuhan, China

Maternal and Child Health Hospital of Hubei Province

Wuhan, China
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Zhang Y.-H.,Huazhong University of Science and Technology | He M.,Maternal and Child Health Hospital of Hubei Province | Wang Y.,Maternal and Child Health Hospital of Hubei Province | Liao A.-H.,Huazhong University of Science and Technology
Frontiers in Immunology | Year: 2017

Macrophages are a subset of mononuclear phagocytes of the innate immune system with high plasticity and heterogeneity. At the maternal-fetal interface, macrophages are present in all stages of pregnancy and involved in a variety of activities, including regulation of immune cell activities, decidualization, placental cell invasion, angiogenesis, parturition, and postpartum uterine involution. The activation state and function of uterine-placental macrophages are largely dependent on the local tissue microenvironment. However, disruption of the uterine microenvironment can have profound effects on macrophage activity and subsequently impact pregnancy outcome. Thus, appropriately and timely regulated macrophage polarization has been considered a key determinant of successful pregnancy. Targeting macrophage polarization might be an efficient strategy for maintaining maternal-fetal immune homeostasis and a normal pregnancy. Here, we will review the latest findings regarding the modulators regulating macrophage polarization in healthy pregnancies and pregnancy complications, which might provide a basis for macrophage-centered therapeutic strategies. © 2017 Zhang, He, Wang and Liao.


Zhao C.,Wuhan University | Lu F.,Wuhan University | Chen H.,Wuhan University | Zhao X.,Wuhan University | Sun J.,Maternal and Child Health Hospital of Hubei Province
International Journal of Clinical and Experimental Pathology | Year: 2014

Junctional adhesion molecule A (JAM-A) is a transmembrane protein that belongs to the immunoglobulin (Ig) superfamily. Evidence determines that JAM-A plays a role in numerous cellular processes, including tight junction assembly, leukocyte migration, platelet activation, angiogenesis and virus binding. Recent research suggests that JAM-A is dysregulated in various cancers and is vital for tumor progression. JAM-A is implicated in carcinogenesis via different signal pathways such as TGF-β1 signaling. Furthermore, JAM-A expression in cancers is usually associated with certain outcome of patients and might be a prognostic indicator. In this review, the correlation between JAM-A expression and human cancers will be described.


Sun J.,Maternal and Child Health Hospital of Hubei Province | Gao J.,Wuhan Nano Tumor Diagnosis Engineering Research Center | Hu J.B.,Maternal and Child Health Hospital of Hubei Province | Fan L.F.,Wuhan University | And 3 more authors.
Oncology Reports | Year: 2012

Altered expression of caveolin-1 (Cav-1) is observed in various types of cancers. However, little research has been reported regarding the correlation between the expression of Cav-1 and cervical cancer. Here, we investigated the clinical significance of Cav-1 expression using quantum dot (QD)-based immunofluorescence staining in cervical cancer and its correlation with high-risk human papilloma virus (HPV) infection detected by chromogenic in situ hybridization. Our results showed that the positive rates of Cav-1 protein in normal cervical mucosa, CIN, cervical adenocarcinoma and SCC were: 0, 33, 19 and 55%, respectively. The differences in Cav-1 protein expression in cervical SCC compared to the other three groups were all statistically significant. Absence of stromal Cav-1 protein in 58 cases of cervical SCC was 67%. The positive rates of the Cav-1 protein in tumour and stromal cells of cervical SCC were not correlated with clinicopathological parameters. In the cervical SCC tissues, Cav-1 expression in tumour cells was not associated with stromal Cav-1 expression, but a positive correlation existed with the PCNA protein and high-risk of HPV infection. The results presented here suggest that expression of Cav-1 in the tumour cells, rather than in the stromal tissue surrounding the tumour, may promote cervical SCC cell proliferation, and correlates with high-risk HPV infection.


PubMed | Hubei University, Hubei Engineering University and Maternal and Child Health Hospital of Hubei Province
Type: Journal Article | Journal: International journal of oncology | Year: 2016

Leukemia represents a spectrum of hematological malignancies threatening human health. Resistance to treatments and metastasis of leukemia are the main causes of death in patients. Leukemia stem cells (LSCs) are the initiating cells of leukemia as well as the main source of drug resistance, invasion and metastasis. Consequently, eliminating LSCs is a prerequisite to eradicate leukemia. Preliminary studies in our laboratory have shown that chemokines and their related receptors play an important role in the drug resistance and metastasis of leukemic cells. In this study, we obtained high migration drug-surviving (short term) MOLT4 cells (hMDSCs-MOLT4) with treatment of doxorubicin (DOX) after Transwell assay. Then we detected stem cell-associated molecular markers on hMDSCs-MOLT4 cells and the parental MOLT4 cells by FCM, QPCR, western blotting, H&E staining and immunohisto-chemistry experimental techniques invitro and invivo. Moreover, we explored its impact on drug resistance and tumor formation. Then we found that compared with the parental MOLT4 cells, the mRNA expression levels of stem cell-related factors Sox2, Oct4, C-myc, Klf4, Nanog, Bmi-1, CXCR4 are increased in hMDSCs-MOLT4 cells, together with the protein expression levels of Sox2, Oct4, Klf4, Nanog, CXCR4 and CD34. Our results indicated that hMDSCs-MOLT4 cells exhibited strong drug resistance and certain cancer stem cell-like characteristics. It is the first indication that the targeting stemness factors such as Sox2, Oct4, Klf4, Nanog and CXCR4 may represent plausible options for eliminating T-ALL stem-like cells. The present findings shed light on the relationship between drug-tolerant leukemic cells and cancer stem cells.


Duan J.,Maternal and Child Health Hospital of Hubei Province | Lang Y.,Maternal and Child Health Hospital of Hubei Province | Song C.,Wuhan General Hospital of Guangzhou Military | Xiong J.,Maternal and Child Health Hospital of Hubei Province | And 2 more authors.
Molecular Medicine Reports | Year: 2013

The overexpression of peroxiredoxins (prxs) has been shown to be associated with the development, progression and drug resistance of cancer. However, the role of the prxs in the drug resistance of ovarian cancer is unknown. The present study aimed to investigate the effect and mechanism of the downregulation of PRDX3 on cisplatin-induced ovarian cancer cell apoptosis. The expression of PRDX3 in ovarian cancer was examined by immunohistochemistry. The effect on cisplatin-induced ovarian cancer apoptosis by the silencing of PRDX3 was determined by cell proliferation and colony formation assays and the examination of tumor growth in the nude mice. To further investigate the mechanism behind the downregulation of PRDX3, the expression of the anti-apoptotic proteins Bcl-2 and Bcl-XL and the pro-apoptotic proteins Bax, Caspase-3 and Caspase-9 was examined in various ovarian cancer cells. The results showed that the aberrant expression of PRDX3 in ovarian cancer may be a factor responsible for its progression. SKOV3 ovarian cancer cells transfected with PRDX3/small interfering (Si)-1 efficiently downregulated the expression of PRDX3 and thus decreased the growth of the SKOV3 cells in vitro and in vivo. Furthermore, the silencing of PRDX3 triggered cisplatin-mediated apoptosis in the ovarian cancer cells, which may act through suppression of the NF-κB signaling pathway. These data suggest a new mechanism by which the downregulation of PRDX3 enhances cisplatin-induced ovarian cancer cell apoptosis. This mechanism may provide new evidence for the potential application of PRDX3-siRNA in ovarian cancer therapy.


Liu X.,CAS Wuhan Institute of Hydrobiology | Chen Z.,CAS Wuhan Institute of Hydrobiology | Chen Z.,Maternal and Child Health Hospital of Hubei Province | Xu C.,CAS Wuhan Institute of Hydrobiology | And 4 more authors.
Nucleic Acids Research | Year: 2015

Hypoxia-inducible factor (HIF)-1α and HIF-2α are the main regulators of cellular responses to hypoxia. Post-translational modifications of HIF-1α and 2α are necessary to modulate their functions. The methylation of non-histone proteins by Set7, an SET domain-containing lysine methyltransferase, is a novel regulatory mechanism to control cell protein function in response to various cellular stresses. In this study, we show that Set7 methylates HIF-1α at lysine 32 and HIF-2α at lysine K29; this methylation inhibits the expression of HIF-1α/2α targets by impairing the occupancy of HIF-α on hypoxia response element of HIF target gene promoter. Set7-null fibroblasts and the cells with shRNA-knocked down Set7 exhibit upregulated HIF target genes. Set7 inhibitor blocks HIF-1α/2α methylation to enhance HIF target gene expression. Set7-null fibroblasts and the cells with shRNA-knocked down Set7 or inhibition of Set7 by the inhibitor subjected to hypoxia display an increased glucose uptake and intracellular adenosine triphosphate levels. These findings define a novel modification of HIF-1α/2α and demonstrate that Set7-medited lysine methylation negatively regulates HIF-α transcriptional activity and HIF-1α-mediated glucose homeostasis. © 2015 The Author(s). Published by Oxford University Press on behalf of Nucleic Acids Research.


Yao Y.,Maternal and Child Health Hospital of Hubei Province | Song J.,Maternal and Child Health Hospital of Hubei Province | Wang W.,Maternal and Child Health Hospital of Hubei Province | Liu N.,Maternal and Child Health Hospital of Hubei Province
Immunology and Cell Biology | Year: 2015

Adaptation of the maternal immune response to accommodate the semiallogeneic fetus is necessary for pregnancy success. However, the mechanisms by which the fetus avoids rejection despite expression of paternal alloantigens remain incompletely understood. Regulatory T cells (Treg cells) are pivotal for maintaining immune homeostasis, preventing autoimmune disease and fetus rejection. In this study, we found that maternal decidual vascular endothelial cells (DVECs) sustained Foxp3 expression in resting Treg cells in vitro. Moreover, under in vitro Treg cell induction condition with agonistic antibodies and transforming growth factor (TGF)-β, DVECs promoted Treg cell differentiation from non-Treg conventional T cells. Consistent with the promotion of Treg cell maintenance and differentiation, Treg cell-associated gene expression such as TGF-β, Epstein–Barr-induced gene-3, CD39 and glucocorticoid-induced tumor necrosis factor receptor was also increased in the presence of DVECs. Further study revealed that DVECs expressed Notch ligands such as Jagged-1, Delta-like protein 1 (DLL-1) and DLL-4, while Treg cells expressed Notch1 on their surface. The effects of DVECs on Treg cells was inhibited by siRNA-induced knockdown of expression of Jagged-1 and DLL-1 in DVECs. Downregulation of Notch1 in Treg cells using lentiviral shRNA transduction decreased Foxp3 expression in Treg cells. Adoptive transfer of Notch1-deficient Treg cells increased abortion rate in a murine semiallogeneic pregnancy model. Taken together, our study suggests that maternal DVECs are able to maintain decidual Treg cell identity and promote Treg cell differentiation through activation of Notch1 signal pathway in Treg cells and subsequently inhibit the immune response against semiallogeneic fetuses and preventing spontaneous abortion.Immunology and Cell Biology advance online publication, 19 January 2016; doi:10.1038/icb.2015.119. © 2015 Australasian Society for Immunology Inc.


Yue C.-J.,Maternal and Child Health Hospital of Hubei Province | Feng L.,Huazhong University of Science and Technology | Huang Q.,Huazhong University of Science and Technology
International Journal of Clinical and Experimental Pathology | Year: 2014

Pseudorabies virus (PRV)-614 was injected into the tracheal wall of male MC4R-GFP transgenic mice, resulting in retrograde infections in spinal cord and autonomic premotor areas of the brain including the rostroventrolateral medulla (RVLM). This polysynaptic pathway to the airway may form the substrate underlying the impact of IML and RVLM on airway function. The neurochemical phenotype of MC4R-GFP-positive neurons was identified using fluorescence immunocytochemical labeling. PRV-614/MC4R-GFP dual labeled neurons were detected in spinal IML and the rostral ventrolateral medulla (RVLM). These data demonstrate the RVLM-IML pathway of synaptically connected neurons extending to the airway through melanocortinergic-sympathetic signaling.


PubMed | Maternal and Child Health Hospital of Hubei province, Yale University and Huazhong University of Science and Technology
Type: | Journal: Scientific reports | Year: 2016

The programmed cell death-1(PD-1)/PD-ligand 1 (PD-L1) pathway is critical to immune homeostasis by promoting regulatory T (Treg) development and inhibiting effector T (such as Th17) cell responses. However, the association between the PD-1/PD-L1 pathway and the Treg/Th17 imbalance has not been fully investigated in pre-eclampsia (PE). In this study, we observed an inverse correlation between the percentages of Treg and Th17 cells, and the expression of PD-1 and PD-L1 on the two subsets also changed in PE compared with normal pregnancy. We further explored their relationship in vivo using the L-NG-Nitroarginine Methyl Ester (L-NAME) induced PE-like rat models, also characterized by Treg/Th17 imbalance. Administration of PD-L1-Fc protein provides a protective effects on the pre-eclamptic models, both to the mother and the fetuses, by reversing Treg/Th17 imbalance through inhibiting PI3K/AKT/m-TOR signaling and enhancing PTEN expression. In addition, we also observed a protective effect of PD-L1-Fc on the placenta by reversing placental damages. These results suggested that altered PD-1/PD-L1 pathway contributed to Treg/Th17 imbalance in PE. Treatment with PD-L1-Fc posed protective effects on pre-eclamptic models, indicating that the use of PD-L1-Fc might be a potential therapeutic target in PE treatment.


PubMed | Maternal and Child Health Hospital of Hubei Province
Type: Journal Article | Journal: Immunology and cell biology | Year: 2016

Adaptation of the maternal immune response to accommodate the semiallogeneic fetus is necessary for pregnancy success. However, the mechanisms by which the fetus avoids rejection despite expression of paternal alloantigens remain incompletely understood. Regulatory T cells (Treg cells) are pivotal for maintaining immune homeostasis, preventing autoimmune disease and fetus rejection. In this study, we found that maternal decidual vascular endothelial cells (DVECs) sustained Foxp3 expression in resting Treg cells in vitro. Moreover, under in vitro Treg cell induction condition with agonistic antibodies and transforming growth factor (TGF)-, DVECs promoted Treg cell differentiation from non-Treg conventional T cells. Consistent with the promotion of Treg cell maintenance and differentiation, Treg cell-associated gene expression such as TGF-, Epstein-Barr-induced gene-3, CD39 and glucocorticoid-induced tumor necrosis factor receptor was also increased in the presence of DVECs. Further study revealed that DVECs expressed Notch ligands such as Jagged-1, Delta-like protein 1 (DLL-1) and DLL-4, while Treg cells expressed Notch1 on their surface. The effects of DVECs on Treg cells was inhibited by siRNA-induced knockdown of expression of Jagged-1 and DLL-1 in DVECs. Downregulation of Notch1 in Treg cells using lentiviral shRNA transduction decreased Foxp3 expression in Treg cells. Adoptive transfer of Notch1-deficient Treg cells increased abortion rate in a murine semiallogeneic pregnancy model. Taken together, our study suggests that maternal DVECs are able to maintain decidual Treg cell identity and promote Treg cell differentiation through activation of Notch1 signal pathway in Treg cells and subsequently inhibit the immune response against semiallogeneic fetuses and preventing spontaneous abortion.

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