A5101778762- Parkinson's Disease Mechanisms and Treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Nuclear Receptors and Signaling
- Nerve injury and regeneration
- Trace Elements in Health
- Heavy Metal Exposure and Toxicity
- Alzheimer's disease research and treatments
- Neurological diseases and metabolism
- RNA regulation and disease
- Inflammasome and immune disorders
- Neuroscience and Neuropharmacology Research
- Genetic Mapping and Diversity in Plants and Animals
- Adenosine and Purinergic Signaling
- Prion Diseases and Protein Misfolding
- Neurological disorders and treatments
- Mitochondrial Function and Pathology
- Histone Deacetylase Inhibitors Research
- Extracellular vesicles in disease
- Chromosomal and Genetic Variations
- Plant Disease Resistance and Genetics
- Botulinum Toxin and Related Neurological Disorders
- Autophagy in Disease and Therapy
- Endoplasmic Reticulum Stress and Disease
- RNA Interference and Gene Delivery
- Vanadium and Halogenation Chemistry
University of Georgia
2022-2025
Neurological Surgery
2024
Iowa State University
2014-2023
Ames National Laboratory
2014
Obstetrics and Gynecology Hospital of Fudan University
2010-2012
Second Military Medical University
2009
Zhejiang Sci-Tech University
2008
Wuhan University
2005-2008
Seoul National University
2007
Chinese Academy of Sciences
2006
The NLRP3 inflammasome signaling pathway is a major contributor to the neuroinflammatory process in central nervous system. Oxidative stress and mitochondrial dysfunction are key pathophysiological processes of many chronic neurodegenerative diseases, including Parkinson's disease (PD). However, inter-relationship between defects neuroinflammation not well understood. In present study, we show that impaired function can augment inflammasome-driven proinflammatory cascade microglia. Primary...
Persistent microglia-mediated neuroinflammation is a major pathophysiological contributor to the progression of Parkinson’s disease (PD), but cell-signaling mechanisms governing chronic are not well understood. Here, we show that Fyn kinase, in conjunction with class B scavenger receptor CD36, regulates microglial uptake aggregated human α-synuclein (αSyn), which component PD-associated Lewy bodies. αSyn can effectively mediate LPS-independent priming and activation NLRP3 inflammasome....
Abstract Quercetin, one of the major flavonoids in plants, has been recently reported to have neuroprotective effects against neurodegenerative processes. However, since molecular signaling mechanisms governing these are not well clarified, we evaluated quercetin's effect on events dopaminergic neuronal models and further tested its efficacy MitoPark transgenic mouse model Parkinson's disease ( PD ). Western blot analysis revealed that quercetin significantly induced activation two cell...
We recently demonstrated that protein kinase Cδ (PKCδ), an important member of the novel PKC family, is a key oxidative stress-sensitive can be activated by caspase-3-dependent proteolytic cleavage to induce dopaminergic neuronal cell death. now report association between α-synuclein (αsyn), associated with pathogenesis Parkinson's disease, and PKCδ, in which αsyn negatively modulates p300- nuclear factor-κB (NFκB)-dependent transactivation downregulate proapoptotic PKCδ expression thereby...
Sustained neuroinflammation mediated by resident microglia is recognized as a key pathophysiological contributor to many neurodegenerative diseases, including Parkinson9s disease (PD), but the molecular signaling events regulating persistent microglial activation have yet be clearly defined. In present study, we examined role of Fyn, non-receptor tyrosine kinase, in and neuroinflammatory mechanisms cell culture animal models PD. The well-characterized inflammogens LPS TNFα rapidly activated...
Manganese exposure promotes α-synuclein propagation, neuroinflammation, and neurodegeneration.
Exosomes containing the adaptor ASC spread NLRP3 inflammasome activation between cells after manganese exposure.
Chronic manganese (Mn) exposure induces neurotoxicity, which is characterized by Parkinsonian symptoms resulting from impairment in the extrapyramidal motor system of basal ganglia. Mitochondrial dysfunction and oxidative stress are considered key pathophysiological features Mn neurotoxicity. Recent evidence suggests astrocytes as a major target neurotoxicity since accumulates predominantly astrocytes. However, primary mechanisms underlying Mn-induced astroglial its role metal not completely...
Abstract Astrocyte reactivity is disease‐ and stimulus‐dependent, adopting either a proinflammatory A1 phenotype or protective, anti‐inflammatory A2 phenotype. Recently, we demonstrated, using cell culture, animal models human brain samples, that dopaminergic neurons produce secrete higher levels of the chemokine‐like signaling protein Prokineticin‐2 (PK2) as compensatory protective response against neurotoxic stress. As astrocytes express high level PK2 receptors, herein, systematically...
Aims: Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive motor deficits and degeneration of dopaminergic neurons. Caused number genetic environmental factors, mitochondrial dysfunction oxidative stress play role in neurodegeneration PD. By selectively knocking out transcription factor A (TFAM) neurons, the transgenic MitoPark mice recapitulate many signature features disease, including deficits, neuronal loss, protein inclusions. In present study, we...
Identification of a peripheral biomarker is major roadblock in the diagnosis PD. Immunohistological identification p-serine 129 α-synuclein submandibular gland tissues PD patients has been recently reported.
An unmet clinical need in Parkinson's disease (PD) is to identify biomarkers for diagnosis, preferably peripherally accessible tissues such as skin. Immunohistochemical studies have detected pathological α-synuclein (αSyn) skin biopsies from PD patients albeit sensitivity needs be improved.
Characterization of the key cellular targets contributing to sustained microglial activation in neurodegenerative diseases, including Parkinson's disease (PD), and optimal modulation these can provide potential treatments halt progression. Here, we demonstrated that Kv1.3, a voltage-gated potassium channel, was transcriptionally upregulated response aggregated α-synuclein (αSynAgg) stimulation primary cultures animal models PD, as well postmortem human PD brains. Patch-clamp...
The pathological role of α-synuclein (α-Syn) aggregation in neurodegeneration is well recognized, but the physiological function normal α-Syn remains unknown. As protein contains multiple divalent metal binding sites, herein we conducted a comprehensive characterization manganese-induced dopaminergic neurotoxicity. We established transgenic N27 neuronal cells by stably expressing human wild-type at levels. α-Syn-expressing significantly attenuated Mn-induced neurotoxicity for 24-h exposures...