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14 results on '"Cao, Meiwan"'

3. The transcription factor ELF4 alleviates inflammatory bowel disease by activating IL1RN transcription, suppressing inflammatory TH17 cell activity, and inducing macrophage M2 polarization

Author

Cao, Meiwan, primary, Chen, Peiyu, additional, Peng, Baoling, additional, Cheng, Yang, additional, Xie, Jing, additional, Hou, Ziang, additional, Chen, Huan, additional, Ye, Liping, additional, Li, Huiwen, additional, Wang, Hongli, additional, Ren, Lu, additional, Xiong, Liya, additional, Geng, Lanlan, additional, and Gong, Sitang, additional

Published
2023
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5. miR-155-5p PROMOTES CD34+ APOPTOSIS AND INHIBITS BONE MARROW HEMATOPOIESIS IN MYELODYSPLASTIC SYNDROMES BY RAC1/CREB/MIR-15B AXIS

Author

Cao, Meiwan, primary, Peng, BaoLing, additional, Xu, WanFu, additional, Chen, PeiYu, additional, Chen, Huan, additional, Ye, LiPing, additional, Xie, Jing, additional, Wang, HongLi, additional, Ren, Lu, additional, Xiong, LiYa, additional, Zhu, JingNan, additional, Xu, XiangYe, additional, Geng, LanLan, additional, and Gong, SiTang, additional

Published
2023
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6. miR-34a induces neutrophil apoptosis by regulating Cdc42-WASP-Arp2/3 pathway-mediated F-actin remodeling and ROS production

Author

Cao, Meiwan, primary, Peng, Baoling, additional, Chen, Huan, additional, Yang, Min, additional, Chen, Peiyu, additional, Ye, Liping, additional, Wang, Hongli, additional, Ren, Lu, additional, Xie, Jing, additional, Zhu, Jingnan, additional, Xu, Xiangye, additional, Xu, Wanfu, additional, Geng, Lanlan, additional, and Gong, Sitang, additional

Published
2022
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8. Mast cells-derived MiR-223 destroys intestinal barrier function by inhibition of CLDN8 expression in intestinal epithelial cells

Author

Li,Musheng, Zhao,Junhong, Cao,Meiwan, Liu,Ruitao, Chen,Guanhua, Li,Songyu, Xie,Yuanwen, Xie,Jing, Cheng,Yang, Huang,Ling, Su,Mingmin, Xu,Yuxin, Zheng,Mingyue, Zou,Kejian, Geng,Lanlan, Xu,Wanfu, Gong,Sitang, Li,Musheng, Zhao,Junhong, Cao,Meiwan, Liu,Ruitao, Chen,Guanhua, Li,Songyu, Xie,Yuanwen, Xie,Jing, Cheng,Yang, Huang,Ling, Su,Mingmin, Xu,Yuxin, Zheng,Mingyue, Zou,Kejian, Geng,Lanlan, Xu,Wanfu, and Gong,Sitang

Abstract

Background: Mast cells (MCs) have been found to play a critical role during development of inflammatory bowel disease (IBD) that characterized by dysregulation of inflammation and impaired intestinal barrier function. However, the function of MCs in IBD remains to be fully elucidated. Results: In our study, we used exosomes isolated from human mast cells-1 (HMCs-1) to culture with NCM460, HT-29 or CaCO2 of intestinal epithelial cells (lECs) to investigate the communication between MCs and lECs. We found that MCs-derived exosomes significantly increased intestinal epithelial permeability and destroyed intestinal barrier function, which is attributed to exosome-mediated functional miRNAs were transferred from HMCs-1 into lECs, leading to inhibit tight junction-related proteins expression, including tight junction proteins 1 (TJP1, ZO-1), Occludin (OCLN), Claudin 8 (CLDN8). Microarray and bioinformatic analysis have further revealed that a panel of miRNAs target different tight junction-related proteins. Interestingly, miR-223 is enriched in mast cell-derived exosome, which inhibit CLDN8 expression in IECs, while treatment with miR-223 inhibitor in HT-29 cells significantly reversed the inhibitory effect of HMCs-1-derived exosomes on CLDN 8 expression. Most importantly, enrichment of MCs accumulation in intestinal mucosa of patients with IBD compared with those healthy control. Conclusions: These results indicated that enrichment of exosomal miR-223 from HMCs-1 inhibited CLDN8 expression, leading to destroy intestinal barrier function. These finding provided a novel insight of MCs as a new target for therapeutic treatment of IBD.

Published
2020

9. Inhibition of CREB‐mediated ZO‐1 and activation of NF‐κB‐induced IL‐6 by colonic epithelial MCT4 destroys intestinal barrier function

Author

Zhang, Shunxian, primary, Xu, Wanfu, additional, Wang, Hongli, additional, Cao, Meiwan, additional, Li, Musheng, additional, Zhao, Junhong, additional, Hu, Yan, additional, Wang, Yaodong, additional, Li, Songyu, additional, Xie, Yuanwen, additional, Chen, Guanhua, additional, Liu, Ruitao, additional, Cheng, Yang, additional, Xu, Zhaohui, additional, Zou, Kejian, additional, Gong, Sitang, additional, and Geng, Lanlan, additional

Published
2019
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11. Reduction of c-Fos via Overexpression of miR-34a Results in Enhancement of TNF- Production by LPS in Neutrophils from Myelodysplastic Syndrome Patients

Author

Shikama, Yayoi, primary, Cao, Meiwan, additional, Ono, Tomoyuki, additional, Feng, Xiaomin, additional, Noji, Hideyoshi, additional, Kimura, Hideo, additional, Ogawa, Kazuei, additional, Suzuki, Yuko, additional, Ikeda, Kazuhiko, additional, Takeishi, Yasuchika, additional, and Kimura, Junko, additional

Published
2016
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12. Excessive TNF-α Production Results from Reduction of c-Fos Via Aberrant Expression of Mir-34a in Neutrophils from Myelodysplastic Syndrome Patients

Author

Shikama, Yayoi, primary, Cao, Meiwan, additional, Ono, Tomoyuki, additional, Anzai, Michiko, additional, Noji, Hideyoshi, additional, Feng, Xiaomin, additional, Kimura, Hideo, additional, Ogawa, Kazuei, additional, Ikeda, Kazuhiko, additional, Takeishi, Yasuchika, additional, and Kimura, Junko, additional

Published
2015
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14. The Mechanism of miR-155/miR-15b Axis Contributed to Apoptosis of CD34+ Cells by Upregulation of PD-L1 in Myelodysplastic Syndromes.

Author

Cao M, Peng B, Xu W, Chen P, Li H, Cheng Y, Chen H, Ye L, Xie J, Wang H, Ren L, Xiong L, Zhu J, Xu X, Geng L, and Gong S

Abstract

Myelodysplastic syndromes (MDS) are a group of heterogeneous myeloid clonal diseases that are characterized by ineffective bone marrow hematopoiesis. Since studies have confirmed the significance of miRNAs in ineffective hematopoiesis in MDS, the current report elucidated the mechanism mediated by miR-155-5p. The bone marrow of MDS patients was collected to detect miR-155-5p and to analyze the correlation between miR-155-5p and clinicopathological variables. Isolated bone marrow CD34+ cells were transfected with lentiviral plasmids that interfere with miR-155-5p, followed by apoptosis analysis. Finally, miR-155-5p-targeted regulation of RAC1 expression was identified, as well as the interaction between RAC1 and CREB, the co-localization of RAC1 and CREB, and the binding of CREB to miR-15b. As measured, miR-155-5p was upregulated in the bone marrow of MDS patients. Further cell experiments validated that miR-155-5p promoted CD34+ cell apoptosis. miR-155-5p could reduce the transcriptional activity of miR-15b by inhibiting RAC1, dissociating the interaction between RAC1 and CREB, and inhibiting the activation of CREB. Upregulating RAC1, CREB, or miR-15b could reduce miR-155-5p-mediated apoptosis promotion on CD34+ cells. Additionally, miR-155-5p could force PD-L1 expression, and this effect was impaired by elevating RAC1, CREB, or miR-15b. In conclusion, miR-155-5p mediates PD-L1-mediated apoptosis of CD34+ cells in MDS by RAC1/CREB/miR-15b axis, thereby inhibiting bone marrow hematopoiesis., Competing Interests: Competing interests: The authors declare no conflict of Interest.

Published
2023
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