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4 results on '"Zhiqun Wang"'

1. TGF-β3-induced miR-494 inhibits macrophage polarization via suppressing PGE2 secretion in mesenchymal stem cells

Author

Yayi Hou, Yali Hu, Zhiqun Wang, Guangfeng Zhao, Huishuang Miao, Shiwen Chen, and Xiujun Li

Subjects
0301 basic medicine, Adult, Biophysics, Macrophage polarization, Biology, Biochemistry, Dinoprostone, 03 medical and health sciences, Young Adult, Transforming Growth Factor beta3, Pre-Eclampsia, Structural Biology, Pregnancy, microRNA, Genetics, medicine, Decidua, Macrophage, Humans, Secretion, Molecular Biology, Cells, Cultured, Regulation of gene expression, Macrophages, Mesenchymal stem cell, Cell Polarity, Mesenchymal Stem Cells, Cell Biology, Macrophage Activation, M2 Macrophage, Cell biology, MicroRNAs, 030104 developmental biology, medicine.anatomical_structure, Gene Expression Regulation, Maternal-Fetal Relations, Female
Abstract

Abnormal macrophage polarization at the maternal-fetal interface may contribute to the development of Preeclampsia (PE). The reason why macrophage polarization changed in PE is still unclear. Decidual mesenchymal stem cells (dMSCs) could regulate macrophage polarization. However, miRNA in dMSCs of PE were maladjusted. Therefore, we speculated that miRNA may affect dMSC-regulated macrophage polarization. In this study, we found that miR-494-overexpressed dMSCs inhibit M2 macrophage polarization and this inhibitory effect is mediated by miR-494-reduced PGE2 secretion. Furthermore, we proved that miR-494 is induced by TGF-β3. In summary, our findings suggest that the high expression of TGF-β3 in PE decidua stimulates miR-494 in dMSCs and attenuates the regulation of MSC switching the macrophage toward M2 type, contributing to an immune imbalance at maternal-fetal interface.

Published
2016

2. TGF-β3-induced miR-494 inhibits macrophage polarization via suppressing PGE2 secretion in mesenchymal stem cells.

Author

Guangfeng Zhao, Huishuang Miao, Xiujun Li, Shiwen Chen, Yali Hu, Zhiqun Wang, and Yayi Hou

Subjects
TRANSFORMING growth factors, PREECLAMPSIA, MESENCHYMAL stem cells, MACROPHAGES, MATERNAL-fetal exchange, GENETIC overexpression
Abstract

Abnormal macrophage polarization at the maternal-fetal interface may contribute to the development of Preeclampsia (PE). The reason why macrophage polarization changed in PE is still unclear. Decidual mesenchymal stem cells (dMSCs) could regulate macrophage polarization. However, miRNA in dMSCs of PE were maladjusted. Therefore, we speculated that miRNA may affect dMSC-regulated macrophage polarization. In this study, we found that miR-494-overexpressed dMSCs inhibit M2 macrophage polarization and this inhibitory effect is mediated by miR-494-reduced PGE2 secretion. Furthermore, we proved that miR-494 is induced by TGF-β3. In summary, our findings suggest that the high expression of TGF-b3 in PE decidua stimulates miR-494 in dMSCs and attenuates the regulation of MSC switching the macrophage toward M2 type, contributing to an immune imbalance at maternal-fetal interface. [ABSTRACT FROM AUTHOR]

Published
2016
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3. MicroRNA-494 inhibits the growth and angiogenesis-regulating potential of mesenchymal stem cells

Author

Yayi Hou, Yali Hu, Yuxian Song, Shiwen Chen, Huishuang Miao, Ruijing Tang, Zhiqun Wang, and Guangfeng Zhao

Subjects
Vascular Endothelial Growth Factor A, Angiogenesis, Biophysics, Gene Expression, Neovascularization, Physiologic, Apoptosis, Biochemistry, chemistry.chemical_compound, Cyclin D1, Cyclin D2, Pre-Eclampsia, Structural Biology, Cell Movement, Pregnancy, microRNA, Genetics, Decidua, Human Umbilical Vein Endothelial Cells, Humans, Molecular Biology, Cells, Cultured, Cell Proliferation, Mesenchymal stem cell, Binding Sites, biology, Base Sequence, Mesenchymal Stem Cells, Cell Biology, Preeclampsia, Molecular biology, G1 Phase Cell Cycle Checkpoints, Cell biology, Vascular endothelial growth factor, Cyclin E1, MicroRNAs, chemistry, biology.protein, Female, RNA Interference, Cyclin-dependent kinase 6, microRNA-494-3p
Abstract

Mesenchymal stem cells (MSCs) play an important role in the pathology of preeclampsia (PE). Our previous microarray analysis found that microRNA-494 (miR-494) is highly expressed in decidua-derived MSCs (dMSCs) from PE. We hypothesized that aberrant expression of miR-494 in dMSCs is involved in PE development. In the present study, we found that miR-494 arrests G1/S transition in dMSCs by targeting CDK6 and CCND1. We also found that supernatant from miR-494-overexpressing dMSCs reduces HTR-8/SVneo migration and impairs HUVEC capillary formation by suppressing VEGF. Taken together, we report an unrecognized mechanism of miR-494 affecting dMSC proliferation and function in the pathology of PE.

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4. FSH acts on the proliferation of type A spermatogonia via Nur77 that increases GDNF expression in the Sertoli cells

Author

Zhenyu Diao, Zhiqun Wang, Yali Hu, Qiu-Yan Ge, Zhongzhou Yang, Haixiang Sun, Fei Yu, Xia Zhao, Guijun Yan, and Lijun Ding

Subjects
Male, Transcriptional Activation, medicine.medical_specialty, endocrine system, Transcription, Genetic, Nerve growth factor IB, animal diseases, Biophysics, Biochemistry, Glial cell line-derived neurotrophic factor, Mice, Follicle-stimulating hormone, Nur77, Structural Biology, Internal medicine, Nuclear Receptor Subfamily 4, Group A, Member 1, Genetics, medicine, Animals, Humans, Molecular Biology, Cells, Cultured, Cell Proliferation, Messenger RNA, Gene knockdown, Sertoli Cells, biology, Cell growth, urogenital system, A spermatogonia, Cell Biology, NGFI-B response element, Sertoli cell, Spermatogonia, In vitro, Cell biology, Endocrinology, medicine.anatomical_structure, nervous system, biology.protein, Follicle Stimulating Hormone
Abstract

The molecular mechanism responsible for the regulation of GDNF in Sertoli cells remains largely unknown. In the present study, FSH induced the expression of Nur77 and GDNF in mouse testis tissue and human fetal Sertoli cells. Moreover, FSH increased the number of A spermatogonia co-cultured with Sertoli cells. In the additional assays, Nur77 was observed to directly regulate GDNF transcription. Furthermore, overexpression of Nur77 and siRNA-mediated knockdown of Nur77 affected levels of GDNF mRNA and protein in primary human fetal Sertoli cells. These results indicate that FSH-induced Nur77 regulates the expression of GDNF in Sertoli cells to stimulate the proliferation of A spermatogonia in vitro.

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