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137 results on '"Chen, Xinqian"'

4. PTSD Increases Risk for Hypertension Development Through PVN Activation and Vascular Dysfunction in Sprague Dawley Rats.

Author

Chen, Xinqian, Yan, Xin, Yu, Chunxiu, Chen, Qing-hui, Bi, Lanrong, and Shan, Zhiying

Subjects
SPRAGUE Dawley rats, NITRIC-oxide synthases, CARDIOVASCULAR diseases, PARAVENTRICULAR nucleus, POST-traumatic stress disorder, ANGIOTENSIN II
Abstract

This study investigates the impact of single prolonged stress (SPS), a model of post-traumatic stress disorder (PTSD), on cardiovascular responses, hypothalamic paraventricular nucleus (PVN) activity, and vascular function to elucidate the mechanisms linking traumatic stress to hypertension. Although SPS did not directly cause chronic hypertension in male Sprague Dawley (SD) rats, it induced acute but transient increases in blood pressure and heart rate and significantly altered the expression of hypertension-associated genes, such as vasopressin, angiotensin II type 1 receptor (AT1R), and FOSL1 in the PVN. Notably, mitochondrial reactive oxygen species (mtROS) were predominantly elevated in the pre-autonomic regions of the PVN, colocalizing with AT1R- and FOSL1-expressing cells, suggesting that oxidative stress may amplify sympathetic activation and stress responses. SPS also increased mRNA levels of pro-inflammatory cytokines (TNFα and IL1β) and inducible nitric oxide synthase (iNOS) in the aorta, and impaired vascular reactivity to vasoconstrictor and vasodilator stimuli, reflecting compromised vascular function. These findings suggest that SPS-sensitize neuroendocrine, autonomic, and vascular pathways create a state of cardiovascular vulnerability that could predispose individuals to hypertension when exposed to additional stressors. Understanding these mechanisms provides critical insights into the pathophysiology of stress-related cardiovascular disorders and underscores the need for targeted therapeutic interventions that address oxidative stress and modulate altered PVN pathways to mitigate the cardiovascular impact of PTSD and related conditions. [ABSTRACT FROM AUTHOR]

Published
2024
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25. microRNA-483 Protects Pancreatic β-Cells by Targeting ALDH1A3

Author

Wang, Zhihong, primary, Mohan, Ramkumar, additional, Chen, Xinqian, additional, Matson, Katy, additional, Waugh, Jackson, additional, Mao, Yiping, additional, Zhang, Shungang, additional, Li, Wanzhen, additional, Tang, Xiaohu, additional, Satin, Leslie S, additional, and Tang, Xiaoqing, additional

Published
2021
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26. Proteomic Profiling of Cerebrum Mitochondria, Myelin Sheath, and Synaptosome Revealed Mitochondrial Damage and Synaptic Impairments in Association with 3 × Tg‐AD Mice Model

Author

Shen, Liming, primary, Yang, Aochu, additional, Chen, Xinqian, additional, Xiao, Shifeng, additional, Liu, Xukun, additional, Lin, Jing, additional, Zhao, Yuxi, additional, Zhang, Kaoyuan, additional, Li, Cuihua, additional, Ke, Junyan, additional, Zhang, Huajie, additional, and Khan, Naseer Ullah, additional

Published
2021
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35. Alendronate treatment in the revision setting, with and without controlled implant motion

Author

Søballe, Kjeld, Chen, Xinqian, Jensen, Thomas B, Kidder, Louis, and Bechtold, Joan E

Abstract

Introduction Bisphosphonates have been proposed to delay or prevent loosening of joint replacement implants by reducing bone resorption. It is known, however, that implant motion prevents the bone anchorage necessary to maintain secure implant fixation. Methods We used our experimental implant model with controlled motion to evaluate the relative effects of implant motion and bisphosphonate. We implemented our established 8-week experimental revision protocol to obtain a bony and soft tissue setting of revision joint replacement in 16 dogs. At 8 weeks, we had stabilized half of the implants. The other half of the implants continued pistoning. Half of the dogs were exposed to alendronate (oral). Results Stabilization of the revision implant was more effective at improving fixation (higher shear strength) than administering alendronate. As expected, the fibrous membrane remained under unstable conditions, even with alendronate. With alendronate and stabilized implants, increased bone was observed near the sclerotic shell of the revision cavity, but it was reduced with alendronate when the implant was unstable. Interpretation Our findings suggest that it may be difficult for alendronate administration alone to rescue implants that are already loose. In implants that have not progressed to loosening, alendronate may increase bone density at the border with the sclerotic shell, but the effect of this bone in delaying eventual loosening is not known. Udgivelsesdato: 2007-Dec

Published
2007
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49. A Novel Cyanine-Based Fluorescent Dye for Targeted Mitochondrial Imaging in Neurotoxic Conditions and In Vivo Brain Studies.

Author

Yan X, Chen X, Hou S, Li X, Ju J, Shan Z, and Bi L

Abstract

Mitochondrial dysfunction is a key feature of neurodegenerative diseases, often preceding symptoms and influencing disease progression. However, real-time in vivo imaging of mitochondria in the brain is limited by existing dyes like MitoTrackers, which struggle with poor tissue penetration, phototoxicity, and inability to cross the blood-brain barrier (BBB). This study introduces Cy5-PEG4, a novel mitochondrial-targeting dye that overcomes these limitations, enabling high-resolution, non-invasive imaging of mitochondrial dynamics. Cy5-PEG4 effectively labels mitochondria in primary neuronal cells exposed to the SARS-CoV-2 RNYIAQVD peptide, revealing dose-dependent alterations in mitochondrial function that may contribute to COVID-19-related neurodegeneration. Importantly, Cy5-PEG4 crosses the BBB without causing neuroinflammation or toxicity, making it a safe tool for in vivo brain imaging and detailed studies of mitochondrial responses. In 3D cultured cells, Cy5-PEG4 captures dynamic changes in mitochondrial distribution and morphology as cell structures mature, highlighting its potential in neurobiological research, diagnostics, and therapeutic development. These findings support Cy5-PEG4 as a powerful tool for studying disease progression, identifying early biomarkers, and evaluating therapeutic strategies in neurodegenerative disorders and COVID-19.

Published
2024
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50. Design, Synthesis, and Biological Evaluation of Novel Mitochondria-targeting Exosomes.

Author

Yan X, Chen X, Shan Z, and Bi L

Abstract

Mitochondrial dysfunction is implicated in both brain tumors and neurodegenerative diseases, leading to various cellular abnormalities that can promote tumor growth and resistance to thera-pies, as well as impaired energy production and compromised neuronal function. Developing targeted therapies aimed at restoring mitochondrial function and improving overall cellular health could potentially be a promising approach to treating these conditions. Brain-derived exosomes (BR-EVs) have emerged as potential drug delivery vessels for neurological conditions. Herein, we report a new method for creating mitochondria-targeting exosomes and test its application in vitro and in vivo.

Published
2023
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