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2. Anti‐CTLA‐4 m2a Antibody Exacerbates Cardiac Injury in Experimental Autoimmune Myocarditis Mice By Promoting Ccl5‐Neutrophil Infiltration.

Author

Wu, Ming‐Ming, Yang, Yan‐Chao, Cai, Yong‐Xu, Jiang, Shuai, Xiao, Han, Miao, Chang, Jin, Xi‐Yun, Sun, Yu, Bi, Xin, Hong, Zi, Zhu, Di, Yu, Miao, Mao, Jian‐Jun, Yu, Chang‐Jiang, Liang, Chen, Tang, Liang‐Liang, Wang, Qiu‐Shi, Shao, Qun, Jiang, Qing‐Hua, and Pan, Zhen‐Wei

Subjects
*IMMUNE checkpoint inhibitors, *HEART injuries, *HEART fibrosis, *IMMUNE response, *TRANSCRIPTOMES
Abstract

The risk for suffering immune checkpoint inhibitors (ICIs)‐associated myocarditis increases in patients with pre‐existing conditions and the mechanisms remain to be clarified. Spatial transcriptomics, single‐cell RNA sequencing, and flow cytometry are used to decipher how anti‐cytotoxic T lymphocyte antigen‐4 m2a antibody (anti‐CTLA‐4 m2a antibody) aggravated cardiac injury in experimental autoimmune myocarditis (EAM) mice. It is found that anti‐CTLA‐4 m2a antibody increases cardiac fibroblast‐derived C‐X‐C motif chemokine ligand 1 (Cxcl1), which promots neutrophil infiltration to the myocarditic zones (MZs) of EAM mice via enhanced Cxcl1‐Cxcr2 chemotaxis. It is identified that the C–C motif chemokine ligand 5 (Ccl5)‐neutrophil subpopulation is responsible for high activity of cytokine production, adaptive immune response, NF‐κB signaling, and cellular response to interferon‐gamma and that the Ccl5‐neutrophil subpopulation and its‐associated proinflammatory cytokines/chemokines promoted macrophage (Mφ) polarization to M1 Mφ. These altered infiltrating landscape and phenotypic switch of immune cells, and proinflammatory factors synergistically aggravated anti‐CTLA‐4 m2a antibody‐induced cardiac injury in EAM mice. Neutralizing neutrophils, Cxcl1, and applying Cxcr2 antagonist dramatically alleviates anti‐CTLA‐4 m2a antibody‐induced leukocyte infiltration, cardiac fibrosis, and dysfunction. It is suggested that Ccl5‐neutrophil subpopulation plays a critical role in aggravating anti‐CTLA‐4 m2a antibody‐induced cardiac injury in EAM mice. This data may provide a strategic rational for preventing/curing ICIs‐associated myocarditis. [ABSTRACT FROM AUTHOR]

Published
2024
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6. Aldosterone-stimulated endothelial epithelial sodium channel (EnNaC) plays a role in cold exposure–induced hypertension in rats

Author

Tang, Liang-Liang, primary, Yang, Xu, additional, Yu, Shu-Qi, additional, Qin, Qi, additional, Xue, Rong, additional, Sun, Yu, additional, Xiao, Han, additional, Shang, An-Qi, additional, Liu, Jia-Qun, additional, Han, Song-Qi, additional, Liang, Chen, additional, Lou, Jie, additional, Wang, Qiu-Shi, additional, Yu, Chang-Jiang, additional, Wu, Ming-Ming, additional, and Zhang, Zhi-Ren, additional

Published
2022
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7. Preparation of Mo2N/TiN Composite Films and Their Surface Enhanced Raman Spectroscopy

Author

王学沛 WANG Xue-pei, 魏恒勇 WEI Heng-yong, 吴明明 WU Ming-ming, 魏颖娜 WEI Ying-na, 陈 颖 CHEN Ying, 李佳双 LI Jia-shuang, 吴振刚 WU Zhen-gang, 刘燕梅 LIU Yan-mei, and 裴 媛 PEI Yuan

Subjects
Radiation, Materials science, Condensed Matter Physics, Electronic, Optical and Magnetic Materials, Nuclear chemistry
Published
2019

8. Homocysteine Causes Endothelial Dysfunction via Inflammatory Factor-Mediated Activation of Epithelial Sodium Channel (ENaC)

Author

Liang, Chen, primary, Wang, Qiu-Shi, additional, Yang, Xu, additional, Zhu, Di, additional, Sun, Yu, additional, Niu, Na, additional, Yao, Jie, additional, Dong, Bi-Han, additional, Jiang, Shuai, additional, Tang, Liang-Liang, additional, Lou, Jie, additional, Yu, Chang-Jiang, additional, Shao, Qun, additional, Wu, Ming-Ming, additional, and Zhang, Zhi-Ren, additional

Published
2021
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11. NaHS or Lovastatin Attenuates Cyclosporine A–Induced Hypertension in Rats by Inhibiting Epithelial Sodium Channels

Author

Wang, Qiu-Shi, primary, Liang, Chen, additional, Jiang, Shuai, additional, Zhu, Di, additional, Sun, Yu, additional, Niu, Na, additional, Yang, Xu, additional, Yang, Yan-Chao, additional, Dong, Bi-Han, additional, Yao, Jie, additional, Yu, Chang-Jiang, additional, Lou, Jie, additional, Tang, Liang-Liang, additional, Wu, Ming-Ming, additional, Zhang, Zhi-Ren, additional, and Ma, He-Ping, additional

Published
2021
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15. Maturity evaluation model of tangerine based on spectral index

Author

叶灵玉 Ye Ling-yu, 孙旭东 Sun Xu-dong, 韩如冰 Han Ru-bing, 朱丹宁 Zhu Dan-ning, 刘燕德 Liu Yande, 吴明明 Wu Ming-ming, 马奎荣 Ma Kui-rong, and 肖怀春 Xiao Huai-chun

Subjects
Maturity (geology), Spectral index, Statistics, Atomic and Molecular Physics, and Optics, Mathematics
Published
2018

20. Lovastatin attenuates hypertension induced by renal tubule‐specific knockout of ATP‐binding cassette transporter A1, by inhibiting epithelial sodium channels

Author

Wu, Ming‐Ming, primary, Liang, Chen, additional, Yu, Xiao‐Di, additional, Song, Bin‐Lin, additional, Yue, Qiang, additional, Zhai, Yu‐Jia, additional, Linck, Valerie, additional, Cai, Yong‐Xu, additional, Niu, Na, additional, Yang, Xu, additional, Zhang, Bao‐Long, additional, Wang, Qiu‐Shi, additional, Zou, Li, additional, Zhang, Shuai, additional, Thai, Tiffany L., additional, Ma, Jing, additional, Sutliff, Roy L., additional, Zhang, Zhi‐Ren, additional, and Ma, He‐Ping, additional

Published
2019
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23. Dietary salt blunts vasodilation by stimulating epithelial sodium channels in endothelial cells from salt‐sensitive Dahl rats

Author

Wang, Zi‐Rui, Liu, Hui‐Bin, Sun, Ying‐Ying, Hu, Qing‐Qing, Li, Yu‐Xia, Zheng, Wei‐Wan, Yu, Chang‐Jiang, Li, Xin‐Yuan, Wu, Ming‐Ming, Song, Bin‐Lin, Mu, Jian‐Jun, Yuan, Zu‐Yi, Zhang, Zhi‐Ren, and Ma, He‐Ping

Subjects
Male, Rats, Inbred Dahl, Nitric Oxide Synthase Type III, urogenital system, Epithelial Sodium Channel Agonists, Endothelial Cells, Blood Pressure, Nitric Oxide, Mesenteric Arteries, Vasodilation, Animals, Themed Section: Research Papers, Sodium Chloride, Dietary, Epithelial Sodium Channels, Cells, Cultured
Abstract

BACKGROUND AND PURPOSE: Our recent studies show that the reduced activity of epithelial sodium channels (ENaC) in endothelial cells accounts for the adaptation of vasculature to salt in Sprague–Dawley rats. The present study examines a hypothesis that enhanced ENaC activity mediates the loss of vasorelaxation in Dahl salt‐sensitive (SS) rats. EXPERIMENTAL APPROACH: We used the cell‐attached patch‐clamp technique to record ENaC activity in split‐open mesenteric arteries. Western blot and immunofluorescence staining were used to evaluate the levels of aldosterone, ENaC, eNOS and NO. Blood pressure was measured with the tail‐cuff method and the artery relaxation was measured with the wire myograph assay. KEY RESULTS: High‐salt (HS) diet significantly increased plasma aldosterone and ENaC activity in the endothelial cells of Dahl SS rats. The endothelium‐dependent artery relaxation was blunted by HS challenge in these rats. Amiloride, a potent blocker of ENaC, increased both phosphorylated eNOS and NO and therefore prevented the HS‐induced loss of vasorelaxation. As, in SS rats, endogenous aldosterone was already elevated by HS challenge, exogenous aldosterone did not further elevate ENaC activity in the rats fed with HS. Eplerenone, a mineralocorticoid receptor antagonist, attenuated the effects of HS on both ENaC activity and artery relaxation. CONCLUSIONS AND IMPLICATIONS: These data suggest that HS diet blunts artery relaxation and causes hypertension via a pathway associated with aldosterone‐dependent activation of ENaC in endothelial cells. This pathway provides one of the mechanisms by which HS causes hypertension in Dahl SS rats. LINKED ARTICLES: This article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc

Published
2017

24. TRUSS Exacerbates NAFLD Development by Promoting IκBα Degradation in Mice

Author

Yu, Chang‐Jiang, primary, Wang, Qiu‐Shi, additional, Wu, Ming‐Ming, additional, Song, Bin‐Lin, additional, Liang, Chen, additional, Lou, Jie, additional, Tang, Liang‐Liang, additional, Yu, Xiao‐Di, additional, Niu, Na, additional, Yang, Xu, additional, Zhang, Bao‐Long, additional, Qu, Yao, additional, Liu, Yang, additional, Dong, Zhi‐Chao, additional, and Zhang, Zhi‐Ren, additional

Published
2018
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25. Oxidized low-density lipoprotein stimulates epithelial sodium channels in endothelial cells of mouse thoracic aorta.

Author

Liang, Chen, Wang, Qiu‐Shi, Yang, Xu, Niu, Na, Hu, Qing‐Qing, Zhang, Bao‐Long, Wu, Ming‐Ming, Yu, Chang‐Jiang, Chen, Xiao, Song, Bin‐Lin, Zhang, Zhi‐Ren, Ma, He‐Ping, Wang, Qiu-Shi, Hu, Qing-Qing, Zhang, Bao-Long, Wu, Ming-Ming, Yu, Chang-Jiang, Song, Bin-Lin, Zhang, Zhi-Ren, and Ma, He-Ping

Subjects
SODIUM channels, VASODILATION, CELLULAR signal transduction, ENDOTHELIAL cells, LOW density lipoproteins, EPITHELIAL cells, CELL receptors, REACTIVE oxygen species, ANIMAL experimentation, COMPARATIVE studies, RESEARCH methodology, MEDICAL cooperation, MICE, RESEARCH, EVALUATION research, IN vitro studies, THORACIC aorta, MEMBRANE transport proteins, PHYSIOLOGY, CELL physiology
Abstract

Background and Purpose: The epithelial sodium channel (ENaC) is expressed in endothelial cells and acts as a negative modulator of vasodilatation. Oxidized LDL (ox-LDL) is a key pathological factor in endothelial dysfunction. In the present study we examined the role of ENaC in ox-LDL-induced endothelial dysfunction and its associated signal transduction pathway.Experimental Approach: Patch clamp techniques combined with pharmacological approaches were used to examine ENaC activity in the endothelial cells of a split-open mouse thoracic aorta. Western blot analysis was used to determine ENaC expression in the aorta. The aorta relaxation was measured using a wire myograph assay.Key Results: Ox-LDL, but not LDL, significantly increased ENaC activity in the endothelial cells attached to split-open thoracic aortas, and the increase was inhibited by a lectin-like ox-LDL receptor-1 (LOX-1) antagonist (κ-carrageenan), an NADPH oxidase inhibitor (apocynin), and a scavenger of ROS (TEMPOL). Sodium nitroprusside, an NO donor, diminished the ox-LDL-mediated activation of ENaC, and this effect was abolished by inhibiting soluble guanylate cyclase (sGC) and PKG. Ox-LDL reduced the endothelium-dependent vasodilatation of the aorta pectoralis induced by ACh, and this reduction was partially restored by blocking ENaC.Conclusion and Implications: Ox-LDL stimulates ENaC in endothelial cells through LOX-1 receptor-mediated activation of NADPH oxidase and accumulation of intracellular ROS. Since the stimulation of ENaC can be reversed by elevating NO, we suggest that both inhibition of ENaC and an elevation of NO may protect the endothelium from ox-LDL-induced dysfunction.Linked Articles: This article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc. [ABSTRACT FROM AUTHOR]

Published
2018
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27. Maturity evaluation model of tangerine based on spectral index

Author

LIU Yan-de, 刘燕德, primary, YE Ling-yu, 叶灵玉, additional, SUN Xu-dong, 孙旭东, additional, HAN Ru-bing, 韩如冰, additional, XIAO Huai-chun, 肖怀春, additional, MA Kui-rong, 马奎荣, additional, ZHU Dan-ning, 朱丹宁, additional, and WU Ming-ming, 吴明明, additional

Published
2018
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30. Dietary salt blunts vasodilation by stimulating epithelial sodium channels in endothelial cells from salt‐sensitive Dahl rats

Author

Wang, Zi‐Rui, primary, Liu, Hui‐Bin, additional, Sun, Ying‐Ying, additional, Hu, Qing‐Qing, additional, Li, Yu‐Xia, additional, Zheng, Wei‐Wan, additional, Yu, Chang‐Jiang, additional, Li, Xin‐Yuan, additional, Wu, Ming‐Ming, additional, Song, Bin‐Lin, additional, Mu, Jian‐Jun, additional, Yuan, Zu‐Yi, additional, Zhang, Zhi‐Ren, additional, and Ma, He‐Ping, additional

Published
2017
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35. Dietary salt blunts vasodilation by stimulating epithelial sodium channels in endothelial cells from salt-sensitive Dahl rats.

Author

Wang, Zi‐Rui, Liu, Hui‐Bin, Sun, Ying‐Ying, Hu, Qing‐Qing, Li, Yu‐Xia, Zheng, Wei‐Wan, Yu, Chang‐Jiang, Li, Xin‐Yuan, Wu, Ming‐Ming, Song, Bin‐Lin, Mu, Jian‐Jun, Yuan, Zu‐Yi, Zhang, Zhi‐Ren, Ma, He‐Ping, Wang, Zi-Rui, Liu, Hui-Bin, Sun, Ying-Ying, Hu, Qing-Qing, Li, Yu-Xia, and Zheng, Wei-Wan

Subjects
SODIUM channels regulation, PHYSIOLOGICAL effects of salts, VASODILATION, ENDOTHELIAL cells, ALDOSTERONE, LABORATORY rats, ANIMAL experimentation, BLOOD pressure, CELL culture, COMPARATIVE studies, EPITHELIAL cells, RESEARCH methodology, MEDICAL cooperation, MESENTERIC artery, MICE, NITRIC oxide, OXIDOREDUCTASES, RESEARCH, SALT, EVALUATION research, MEMBRANE transport proteins, CELL physiology
Abstract

Background and Purpose: Our recent studies show that the reduced activity of epithelial sodium channels (ENaC) in endothelial cells accounts for the adaptation of vasculature to salt in Sprague-Dawley rats. The present study examines a hypothesis that enhanced ENaC activity mediates the loss of vasorelaxation in Dahl salt-sensitive (SS) rats.Experimental Approach: We used the cell-attached patch-clamp technique to record ENaC activity in split-open mesenteric arteries. Western blot and immunofluorescence staining were used to evaluate the levels of aldosterone, ENaC, eNOS and NO. Blood pressure was measured with the tail-cuff method and the artery relaxation was measured with the wire myograph assay.Key Results: High-salt (HS) diet significantly increased plasma aldosterone and ENaC activity in the endothelial cells of Dahl SS rats. The endothelium-dependent artery relaxation was blunted by HS challenge in these rats. Amiloride, a potent blocker of ENaC, increased both phosphorylated eNOS and NO and therefore prevented the HS-induced loss of vasorelaxation. As, in SS rats, endogenous aldosterone was already elevated by HS challenge, exogenous aldosterone did not further elevate ENaC activity in the rats fed with HS. Eplerenone, a mineralocorticoid receptor antagonist, attenuated the effects of HS on both ENaC activity and artery relaxation.Conclusions and Implications: These data suggest that HS diet blunts artery relaxation and causes hypertension via a pathway associated with aldosterone-dependent activation of ENaC in endothelial cells. This pathway provides one of the mechanisms by which HS causes hypertension in Dahl SS rats.Linked Articles: This article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc. [ABSTRACT FROM AUTHOR]

Published
2018
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36. Design and implementation for the elevator public service platform base on internet of things

Author

Wu Ming Ming, Lvqing Yang, He Xiao Li, and Huang Jie

Subjects
Structure (mathematical logic), Elevator, SIMPLE (military communications protocol), Computer Networks and Communications, business.industry, Computer science, media_common.quotation_subject, Intelligent decision support system, Base (topology), Computer security, computer.software_genre, Computer Science Applications, Public service, Software engineering, business, Function (engineering), Internet of Things, computer, Software, Information Systems, media_common
Abstract

Security monitoring based on IOT was applied to the elevator-equipment, it provides great convenience and security for people's daily life. By using the basic theory of software engineering, it mainly analyses and designs functions and modules for the elevator public service platform base on IOT in the paper. On the basis of stating the importance of platform construction, it focuses on expounding the function and the non-function requirements. Then the platform structure is established and different functional modules are divided. And it makes a simple description about related development technologies at the end of the paper.

Published
2016

37. The Polarized Effect of Intracellular Calcium on the Renal Epithelial Sodium Channel Occurs as a Result of Subcellular Calcium Signaling Domains Maintained by Mitochondria

Author

Thai, Tiffany L., primary, Yu, Ling, additional, Galarza-Paez, Laura, additional, Wu, Ming Ming, additional, Lam, Ho Yin Colin, additional, Bao, Hui Fang, additional, Duke, Billie Jeanne, additional, Al-Khalili, Otor, additional, Ma, He-Ping, additional, Liu, Bingchen, additional, and Eaton, Douglas C., additional

Published
2015
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38. Characterization of Cardiac Anoctamin1 Ca2+‐Activated Chloride Channels and Functional Role in Ischemia‐Induced Arrhythmias

Author

Ye, Zhen, primary, Wu, Ming‐Ming, additional, Wang, Chun‐Yu, additional, Li, Yan‐Chao, additional, Yu, Chang‐Jiang, additional, Gong, Yuan‐Feng, additional, Zhang, Jun, additional, Wang, Qiu‐Shi, additional, Song, Bin‐Lin, additional, Yu, Kuai, additional, Hartzell, H. Criss, additional, Duan, Dayue Darrel, additional, Zhao, Dan, additional, and Zhang, Zhi‐Ren, additional

Published
2014
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