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1,247 results on '"Wang, Jufang"'

3. Carbon ions inhibit non-small cell lung cancer cell proliferation by inducing mitochondrial damage

Author

ZHANG Tianyi, YANG Pengfei, WANG Jufang, and ZHOU Heng

Subjects
carbon ion irradiation, mitochondrial damage, mitophagy, mitochondrial apoptosis, Nuclear and particle physics. Atomic energy. Radioactivity, QC770-798, Medical physics. Medical radiology. Nuclear medicine, R895-920
Abstract

We investigated the effects of mitochondrial damage via carbon ion irradiation on the proliferation of human non-small cell lung cancer (A549) cells by monitoring mitochondrial morphological changes, mitochondrial membrane potential transformation, release of membrane-associated proteins, and mitophagy. A549 cell proliferation and activity were monitored by CCK-8 and colony formation assays. Changes in mitochondrial morphology and mitochondrial membrane potential were detected by mitochondrial membrane-specific fluorescence staining. Expression of associated proteins was detected by western blot and real-time quantitative PCR. Annexin V-FITC and PI staining were used to detect cell apoptosis. Mitophagy was detected by immunofluorescence co-localization and western blot. The apoptosis rate of mitochondria-lacking A549 cells after carbon ion irradiation was also quantitated. Irradiation with carbon ions at dose of 4 Gy significantly depressed the proliferation capacity of A549 cells, and induced mitochondrial shrinkage and decreased mitochondrial membrane potential. Levels of mitochondrial membrane protein Bax/Bak, and intermembrane proteins Cyto-C and SMAC were elevated, with increased apoptosis and mitophagy. In cells depleted of mitochondria, carbon ion irradiation exerted no significant effect on A549 cell apoptosis. Carbon ion irradiation can inhibit A549 cell proliferation. The half maximal inhibitory exposure dose is 4 Gy. Carbon ions lose their anti-proliferative function in mitochondria-free A549 cells. In summary, carbon ion irradiation can decrease mitochondrial membrane potential and induce the release of pro-apoptotic proteins, thereby inhibiting A549 cell proliferation.

Published
2024
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35. Bag3 Regulates Mitochondrial Function and the Inflammasome Through Canonical and Noncanonical Pathways in the Heart

Author

Wang, JuFang, Tomar, Dhadendra, Martin, Thomas G., Dubey, Shubham, Dubey, Praveen K., Song, Jianliang, Landesberg, Gavin, McCormick, Michael G., Myers, Valerie D., Merali, Salim, Merali, Carmen, Lemster, Bonnie, McTiernan, Charles F., Khalili, Kamel, Madesh, Muniswamy, Cheung, Joseph Y., Kirk, Jonathan A., and Feldman, Arthur M.

Published
2023
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42. China's public opinion control in the platform era : news, media power, and state-platform collaborative governance

Author

Wang, Jufang

Subjects
JQ Political institutions (Asia, Africa, Australia, Pacific Area, etc.), PN Literature (General)
Abstract

The rise of Chinese digital media platforms (e.g., WeChat, Weibo and Toutiao) in the news sphere has transformed China's news landscape. These private platforms are increasingly sitting at the centre of news production, distribution and consumption, leading to a "platform-centered news ecosystem" in China. Such an ecosystem has brought profound changes to China's media power structure: platforms have become the "battlefields" for shaping public opinion and the central gatekeepers and governors of online news and information; self-media (individual news producers) rise as important news actors; state-controlled news organizations are in relative decline. Based on in-depth interviews with senior people from Chinese platforms and news organizations (some of whom are also self-media operators) and document analysis (e.g. of government regulations, official documents from platforms, media outputs, and third-party reports), this thesis has concluded that, despite bringing some challenges to the Chinese party-state's public opinion control, platforms turn out to be an effective Internet governance tool, rather than a disruptive force, to the state. Given that Chinese platforms are not only passively cooperating, but also actively collaborating with the party-state in public opinion control and wider contexts, this thesis proposes a "collaborative governance" model in relation to China's public opinion control. Under this model, the Chinese party-state only needs to target and control a number of major platforms, which have the technological capabilities and surveillance resources to enforce Internet governance on behalf of the state.

Published
2019

44. Drug inhibition and substrate transport mechanisms of human VMAT2.

Author

Wei, Feiwen, Liu, Huihui, Zhang, Wei, Wang, Jufang, and Zhang, Yanqing

Subjects
MONOAMINE transporters, BIOCHEMICAL substrates, SYNAPTIC vesicles, LIFE sciences, PARKINSON'S disease, SEROTONIN
Abstract

Vesicular monoamine transporter 2 (VMAT2) is crucial for packaging monoamine neurotransmitters into synaptic vesicles, with their dysregulation linked to schizophrenia, mood disorders, and Parkinson's disease. Tetrabenazine (TBZ) and valbenazine (VBZ), both FDA-approved VMAT2 inhibitors, are employed to treat chorea and tardive dyskinesia (TD). Our study presents the structures of VMAT2 bound to substrates serotonin (5-HT) and dopamine (DA), as well as the inhibitors TBZ and VBZ. Utilizing cryo-electron microscopy (cryo-EM), mutagenesis functional assays, and molecular dynamics (MD) simulations, we elucidate the mechanisms of substrate transport and drug inhibition. Our MD simulations indicate potential binding poses of substrate (5-HT) in both cytosol-facing and lumen-facing states, emphasizing the significance of protonation of key acidic residues for substrate release. We demonstrate that TBZ locks VMAT2 in a lumen-facing occluded state, while VBZ stabilizes it in a lumen-facing conformation. These insights enhance our understanding of VMAT2 function and provide valuable insights for the development of novel therapeutic strategies for psychiatric disorders. Vesicular monoamine transporter 2 (VMAT2) plays a pivotal role in the packaging of monoamine neurotransmitters, including serotonin and dopamine, into synaptic vesicles. Here, the authors present the structures of VMAT2 in complex with substrates 5-HT and DA, as well as the inhibitors TBZ and VBZ, providing insights into the mechanisms of transport and inhibition. [ABSTRACT FROM AUTHOR]

Published
2025
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