A5008914078- Mitochondrial Function and Pathology
- Alzheimer's disease research and treatments
- Lung Cancer Treatments and Mutations
- Metabolism and Genetic Disorders
- MicroRNA in disease regulation
- Neuroscience and Neuropharmacology Research
- Parkinson's Disease Mechanisms and Treatments
- Neurogenesis and neuroplasticity mechanisms
- Nerve injury and regeneration
- Circular RNAs in diseases
- Cholinesterase and Neurodegenerative Diseases
- Amyotrophic Lateral Sclerosis Research
- Peptidase Inhibition and Analysis
- Lung Cancer Diagnosis and Treatment
- Lung Cancer Research Studies
- DNA Repair Mechanisms
- Colorectal Cancer Treatments and Studies
- Prostate Cancer Treatment and Research
- ATP Synthase and ATPases Research
- Microtubule and mitosis dynamics
- Genomics and Chromatin Dynamics
- RNA modifications and cancer
- NF-κB Signaling Pathways
- RNA Research and Splicing
- Metabolomics and Mass Spectrometry Studies
Shandong University
2013-2024
Baoding People's Hospital
2024
Shanghai Pulmonary Hospital
2016-2024
Tongji University
2006-2024
Yangtze University
2022
Central South University
2009-2017
The First Affiliated Hospital, Sun Yat-sen University
2016
University of South China
2007-2016
Zhongshan Hospital
2016
Fudan University
2016
Mitochondrial dysfunction is a prominent feature of Alzheimer's disease (AD) neurons. In this study, we explored the involvement an abnormal mitochondrial dynamics by investigating changes in expression fission and fusion proteins AD brain potential cause consequence these neuronal cells. We found that mitochondria were redistributed away from axons pyramidal neurons brain. Immunoblot analysis revealed levels DLP1 (also referred to as Drp1), OPA1, Mfn1, Mfn2 significantly reduced whereas...
Mitochondrial dysfunction is a prominent feature of Alzheimer disease but the underlying mechanism unclear. In this study, we investigated effect amyloid precursor protein (APP) and β on mitochondrial dynamics in neurons. Confocal electron microscopic analysis demonstrated that ≈40% M17 cells overexpressing WT APP (APPwt cells) more than 80% APPswe mutant (APPswe displayed alterations morphology distribution. Specifically, mitochondria exhibited fragmented structure an abnormal distribution...
J. Neurochem. (2012) 120 , 419–429. Abstract Mitochondrial dysfunction is a prominent feature of Alzheimer’s disease (AD) brain. Our prior studies demonstrated reduced mitochondrial number in susceptible hippocampal neurons the brain from AD patients and M17 cells over‐expressing familial AD‐causing amyloid precursor protein (APP) mutant (APPswe). In current study, we investigated whether alterations biogenesis contribute to abnormalities AD. regulated by peroxisome proliferator activator...
MicroRNAs have been considered as a kind of potential novel biomarker for cancer detection due to their remarkable stability in the blood and characteristics expression profile many diseases.We performed microarray-based serum miRNA profiling on twenty nasopharyngeal carcinoma patients at diagnosis along with 20 non-cancerous individuals controls. This was followed by real-time quantitative Polymerase Chain Reaction (RT-qPCR) separate cohort thirty age- matched volunteers. A model...
Selective degeneration of nigrostriatal dopaminergic neurons in Parkinson's disease (PD) can be modeled by the administration neurotoxin 1-methyl-4-phenylpyridinium (MPP(+) ). Because abnormal mitochondrial dynamics are increasingly implicated pathogenesis PD, this study, we investigated effect MPP(+) on and assessed temporal causal relationship with other toxic effects induced neuronal cells. In SH-SY5Y cells, causes a rapid increase fragmentation followed second wave fragmentation, along...
In Alzheimer disease (AD), hyperphosphorylation of tau proteins results in microtubule destabilization and cytoskeletal abnormalities. Our prior ultra-morphometric studies documented a clear reduction microtubules pyramidal neurons AD compared to controls, however, this did not coincide with the presence paired helical filaments. The latter suggests compensatory mechanism(s) that stabilize dynamics despite loss binding stabilization. Microtubules are composed tubulin dimers which subject...
Appropriate mitochondrial transport and distribution are essential for neurons because of the high energy Ca(2+) buffering requirements at synapses. Brain-derived neurotrophic factor (BDNF) plays an role in regulating synaptic transmission plasticity. However, whether how BDNF can regulate still unclear. Here, we find that cultured hippocampal neurons, application 15 min decreased percentage moving mitochondria axons, a process dependent on activation TrkB receptor its downstream PI3K...
Abstract The microtubule‐associated protein tau is abnormally hyperphosphorylated in the brains of individuals with Alzheimer disease and other tauopathies, believed to play a critical role pathogenesis these diseases. While mechanisms leading abnormal phosphorylation remain elusive, recent demonstration reversible during hibernation provides an ideal physiological model study this process vivo . In study, arctic ground squirrels (AGS) were used related hyperphosphorylation. Our data...
Overexpression of serine protease inhibitor Kazal type 1 (SPINK1) defines an aggressive molecular subtype ETS fusion-negative prostate cancer (PCa) patients in western countries. However, how SPINK1 contributes to PCa invasion and metastasis is largely unknown.Fluorescence situ hybridization immunohistochemistry were utilized detect ERG rearrangement, expression, EGFR aberrations a cohort 211 with radical prostatectomy. Real-time quantitative PCR Western blotting used study the transcript...
Abstract Background Leptomeningeal metastasis (LM) of small cell lung cancer (SCLC) is a highly detrimental occurrence associated with severe neurological disorders, lacking effective treatment currently. Proteolysis-targeting chimeric molecules (PROTACs) may provide new therapeutic avenues for podophyllotoxin derivatives-resistant SCLC LM, warranting further exploration. Methods The line H128 expressing luciferase were mutated by MNNG to generate H128-Mut line. After subcutaneous...
Promoter hypermethylation-mediated silencing of tumor suppressor genes (TSGs) is a hallmark oncogenesis. Oxidored-nitro domain-containing protein 1 (NOR1) candidate TSG that downregulated in nasopharyngeal carcinoma (NPC). In the present study, we identified functional NOR1 promoter regulated by heat shock factor and nuclear respiratory 1. The located within CpG island. Hypermethylation this island was found NPC tissue samples cancer cell lines, whereas no aberrant methylation detected...