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Your search keyword '"Dang, Shipeng"' showing total 19 results
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19 results on '"Dang, Shipeng"'

7. Impairment of TRPC1-BK complex in diabetic rat coronary artery

Author

Sun, Manqing, primary, Qian, Lingling, additional, Miao, Lingfeng, additional, Wu, Ying, additional, Liu, Xiaoyu, additional, Dang, Shipeng, additional, Tang, Xu, additional, Zhang, Zhenye, additional, Wang, Chao, additional, Chai, Qiang, additional, Yi, Fu, additional, Hao, Jianfeng, additional, and Wang, Ruxing, additional

Published
2021
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8. Blockade of β-adrenergic signaling suppresses inflammasome and alleviates cardiac fibrosis

Author

Ying Wu, Liu Xiaoyu, Ru-Xing Wang, L L Qian, Tingbo Jiang, Xiao-xi Zhao, Yu Zhiming, Jie Zheng, Zhen-Ye Zhang, Chang-ying Zhang, Li Kulin, and Dang Shipeng

Subjects
0301 basic medicine, chemistry.chemical_classification, Reactive oxygen species, Voltage-dependent calcium channel, Chemistry, Cardiac fibrosis, Stimulation, Inflammasome, General Medicine, 030204 cardiovascular system & hematology, Pharmacology, medicine.disease, In vitro, Blockade, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Heart failure, medicine, cardiovascular system, Original Article, medicine.drug
Abstract

Background Heart failure (HF) is an end-stage syndrome of all structural heart diseases which accompanies the loss of myocardium and cardiac fibrosis. Although the role of inflammasome in cardiac fibrosis has recently been a point of focus, the mechanism of inflammasome activation in HF has not yet been elucidated. Methods In this study, we investigated the expression of inflammasome proteins in a rat thoracic aorta constriction (TAC) model and cultured cardiac fibroblasts with stimulation of norepinephrine (NE). Results Our results showed that levels of inflammasome proteins in the myocardial of TAC rats were elevated. By blocking β-adrenergic signaling in the rats, inflammasome activation was suppressed and heart function was improved. The stimulation of cultured cardiac fibroblasts with NE activated inflammasome in vitro, which was abrogated by the inhibition of the calcium channels and reactive oxygen species (ROS). The activation of inflammasome by NE promoted cardiac fibrosis, whereas the inhibition of the calcium channels, ROS, and inflammasome reduced this effect. Conclusions The present study indicated that activation of inflammasome by β-adrenergic signaling promotes cardiac fibrosis. Therefore, modulation of inflammasome during HF might provide a novel strategy to treat this disease.

Published
2020

13. [Effects and activated mechanism of adenosine triphosphate on BK channel of coronary smooth muscle cells]

Author

Wang, Xiangyun, Wu, Ying, Qian, Lingling, Dang, Shipeng, Ji, Yuan, Xu, Feng, Wang, Meng, Tang, Xu, Yao, Yong, and Wang, Ruxing

Subjects
Rats, Sprague-Dawley, Adenosine Triphosphate, Patch-Clamp Techniques, Myocytes, Smooth Muscle, Animals, Calcium, Heart, Large-Conductance Calcium-Activated Potassium Channels, Coronary Vessels, Muscle, Smooth, Vascular, Rats
Abstract

To explore the effects and activation mechanism of adenosine triphosphate (ATP) on large conductance calcium-activated potassium channel ( BK channel) in coronary artery smooth muscle cells.Coronary smooth muscle cells were isolated by enzyme digestion from Sprague-Dawley rats. And BK currents were recorded by patch clamp technique in whole cell configuration. The effects of ATP on cytosolic calcium concentrations were examined by recording the changes of fluorescence intensity ratios.BK current densities were (137 ± 13) pA/pF and (179 ± 15) pA/pF before and after a perfusion of 1 mmol/L ATP (P0.05). The fluorescence ratios were 2.46 ± 0.08 and 4.04 ± 0.21 (P0.05) before and after 0.5 mmol/L perfusion. After incubating with purine receptor (P2Y1) blocker MRS2179, phospholipase C (PLC) blocker U73122 and inositol triphosphate (IP3) blocker 2-APB, the fluorescence ratios were 2.7 ± 0.06, 2.65 ± 0.12 and 2.69 ± 0.13 respectively. Compared with control group, all fluorescence ratios decreased after incubating with three blockers (P0.05).ATP may elevate intracellular calcium concentration via P2Y1-PLC-IP3 pathway consequently activating BK channel.

Published
2015

16. Autophagy regulates the therapeutic potential of mesenchymal stem cells in experimental autoimmune encephalomyelitis

Author

Dang, Shipeng, primary, Xu, Huanbai, additional, Xu, Congfeng, additional, Cai, Wei, additional, Li, Qian, additional, Cheng, Yiji, additional, Jin, Min, additional, Wang, Ru-Xing, additional, Peng, Yongde, additional, Zhang, Yi, additional, Wu, Changping, additional, He, Xiaozhou, additional, Wan, Bing, additional, and Zhang, Yanyun, additional

Published
2014
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17. Stimulation of TLR4 by LMW-HA Induces Metastasis in Human Papillary Thyroid Carcinoma through CXCR7

Author

Dang, Shipeng, primary, Peng, Yongde, additional, Ye, Lei, additional, Wang, Yanan, additional, Qian, Zhongqing, additional, Chen, Yuqing, additional, Wang, Xiaojing, additional, Lin, Yunzhi, additional, Zhang, Xiaomei, additional, Sun, Xiyan, additional, Wu, Qiong, additional, Cheng, Yiji, additional, Nie, Hong, additional, Jin, Min, additional, and Xu, Huanbai, additional

Published
2013
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19. Protective role of the CD73-A2AR axis in cirrhotic cardiomyopathy through negative feedback regulation of the NF-κB pathway.

Author

Zhao N, Shao Z, Xia G, Liu H, Zhang L, Zhao X, Dang S, Qian L, Xu W, Yu Z, and Wang R

Subjects
Animals, Male, Mice, Apoptosis, Disease Models, Animal, Feedback, Physiological, GPI-Linked Proteins, Mice, Inbred C57BL, NF-kappa B metabolism, 5'-Nucleotidase metabolism, Cardiomyopathies metabolism, Cardiomyopathies etiology, Cardiomyopathies immunology, Liver Cirrhosis immunology, Liver Cirrhosis metabolism, Receptor, Adenosine A2A metabolism, Signal Transduction
Abstract

Background: Myocardial inflammation and apoptosis induced by cirrhosis are among the primary mechanisms of cirrhotic cardiomyopathy. CD73, a common extracellular nucleotidase also known as 5'-nucleotidase, is associated with the progression of inflammation and immunity in multiple organs. However, the mechanism by which CD73 contributes to myocardial inflammation and apoptosis in cirrhosis remains unclear., Methods: In this study, a cirrhotic cardiomyopathy model in mice was established by bile duct ligation. Myocardial-specific overexpression of CD73 was achieved by tail vein injection of AAV9 (adeno-associated virus)-cTNT-NT5E-mCherry, and cardiac function in mice was assessed using echocardiography. Myocardial inflammation infiltration and apoptosis were evaluated through pathological observation and ELISA assays. The expression of CD73, A2AR, apoptotic markers, and proteins related to the NF-κB pathway in myocardial tissue were measured., Results: In the myocardial tissue of the cirrhotic cardiomyopathy mouse model, the expression of CD73 and A2AR increased. Overexpression of CD73 in the myocardium via AAV9 injection and stimulation of A2AR with CGS 21680 inhibited myocardial inflammation and cardiomyocyte apoptosis induced by cirrhosis. Additionally, overexpression of CD73 suppressed the activation of the NF-κB pathway by upregulating the expression of the adenosine receptor A2A., Conclusion: Our study reveals that the CD73/A2AR signaling axis mitigates myocardial inflammation and apoptosis induced by cirrhosis through negative feedback regulation of the NF-κB pathway., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Zhao, Shao, Xia, Liu, Zhang, Zhao, Dang, Qian, Xu, Yu and Wang.)

Published
2024
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