Xiaoguang Li

ORCID: 0000-0002-1726-696X
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Adipose Tissue and Metabolism
  • Neuroscience and Neuropharmacology Research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Nuclear Receptors and Signaling
  • Hormonal Regulation and Hypertension
  • Epigenetics and DNA Methylation
  • Histone Deacetylase Inhibitors Research
  • MicroRNA in disease regulation
  • Memory and Neural Mechanisms
  • Nerve injury and regeneration
  • Amyloidosis: Diagnosis, Treatment, Outcomes
  • RNA modifications and cancer
  • Mesenchymal stem cell research
  • Cellular transport and secretion
  • Stress Responses and Cortisol
  • Neurogenesis and neuroplasticity mechanisms
  • Mitochondrial Function and Pathology
  • Reproductive System and Pregnancy
  • Birth, Development, and Health
  • RNA Research and Splicing
  • Neurological Disease Mechanisms and Treatments
  • Magnesium in Health and Disease
  • Animal Virus Infections Studies
  • Aluminum toxicity and tolerance in plants and animals

Huazhong University of Science and Technology
2016-2025

Union Hospital
2020-2025

Tsinghua University
2024

Shanghai Jiao Tong University
2023

State Key Laboratory of Oncogene and Related Genes
2023

Capital Medical University
2012-2021

Wuhan Union Hospital
2021

Beihang University
2021

Shenzhen Bao'an District People's Hospital
2018

Guangzhou University of Chinese Medicine
2015-2016

Macroautophagy/autophagy deficit induces intracellular MAPT/tau accumulation, the hallmark pathology in Alzheimer disease (AD) and other tauopathies; however, reverse role of MAPT accumulation autophagy neurodegeneration is not clear. Here, we found that overexpression human wild-type full-length MAPT, which models pathologies as seen sporadic AD patients, induced deficits via repression autophagosome-lysosome fusion leading to significantly increased LC3 (microtubule-associated protein 1...

10.1080/15548627.2019.1633862 article EN Autophagy 2019-06-21

δ-secretase, also known as asparagine endopeptidase (AEP) or legumain, is a lysosomal cysteine protease that cleaves both amyloid precursor protein (APP) and tau, mediating the amyloid-β tau pathology in Alzheimer's disease (AD). Here we report therapeutic effect of an orally bioactive brain permeable δ-secretase inhibitor mouse models AD. We performed high-throughput screen identified non-toxic selective inhibitor, termed compound 11, specifically blocks but not other related proteases....

10.1038/ncomms14740 article EN cc-by Nature Communications 2017-03-27

Alzheimer's disease (AD) is characterized by profound synapse loss and impairments of learning memory. Magnesium affects many biochemical mechanisms that are vital for neuronal properties synaptic plasticity. Recent studies have demonstrated the serum brain magnesium levels decreased in AD patients; however, exact role pathogenesis remains unclear. Here, we found intraperitoneal administration sulfate increased protected memory capacities streptozotocin-induced sporadic model rats. We also...

10.1371/journal.pone.0108645 article EN cc-by PLoS ONE 2014-09-30

Abstract Different emotional states lead to distinct behavioural consequences even when faced with the same challenging events. Emotions affect learning and memory capacities, but underlying neurobiological mechanisms remain elusive. Here we establish models of learned helplessness (LHL) hopefulness (LHF) by exposing animals inescapable foot shocks or anticipated avoidance trainings. The LHF show spatial potentiation excitatory monosynaptic upscaling between posterior basolateral amygdale...

10.1038/ncomms11935 article EN cc-by Nature Communications 2016-07-14

Abstract Background Synaptic degeneration occurs in the early stage of Alzheimer's disease (AD) before devastating symptoms, strongly correlated with cognitive decline. Circular RNAs (circRNAs) are abundantly enriched neural tissues, and aberrant expression circRNAs precedes AD significantly clinical dementia severity. However, direct relationship between circRNA dysregulation synaptic impairment remains poorly understood. Methods Hippocampal whole-transcriptome sequencing was performed to...

10.1186/s40035-023-00386-6 article EN cc-by Translational Neurodegeneration 2023-11-28

Proteolytic generation of amyloidogenic amyloid β (Aβ) fragments from the precursor protein (APP) significantly contributes to Alzheimer's disease (AD). Although APP proteolysis can be affected by trafficking through genetically associated AD components such as SORLA, how SORLA functionally interacts with other is yet unclear. Here, we report that SNX27, an endosomal trafficking/recycling factor and a negative regulator γ-secretase complex, binds cytosolic tail form ternary complex APP....

10.1523/jneurosci.0206-16.2016 article EN Journal of Neuroscience 2016-07-27

Abstract Alzheimer's disease (AD) is the most common neurodegenerative disorder and there currently no efficient cure for this devastating disease. Cognitive stimulation can delay memory loss during aging in patients with mild cognitive impairment. In 3 × Tg-AD mice, training decreased neuropathologies transient amelioration of decline. However, neurobiological mechanisms underlying learning-improved capacity are poorly understood. Here, we found Tg2576 mice spatial Morris water maze (MWM)...

10.1038/srep09488 article EN cc-by Scientific Reports 2015-03-30

Accumulation of microtubule-associated protein tau has been observed in the brain aging and tauopathies. Tau was microglia, but its role is not illustrated. By immunofluorescence staining fractal dimension value assay present study, we that microglia were activated brains rats mice during aging, simultaneously, immunoreactivities total phosphorylated significantly enhanced microglia. Furtherly by transient transfection tau40 (human 2N/4R tau) into cultured rat demonstrated expression...

10.1371/journal.pone.0076057 article EN cc-by PLoS ONE 2013-10-11

The impairment of histone acetylation is causally linked to the cognitive decline in Alzheimer's disease (AD). In addition acetyltransferases (HATs) and deacetylases (HDACs), inhibitor (INHAT) can also regulate acetylation. As a key component INHAT, level ANP32A selectively upregulated brain AD patients. Here we investigated whether downregulating rescue AD-like synapse memory deficits.RFP-labeled lentiviral ANP32A-shRNA was infused stereotaxically into hippocampal CA3 region human tau...

10.1186/s13024-017-0178-8 article EN cc-by Molecular Neurodegeneration 2017-05-04

Sepsis consists of life-threatening multi-organ dysfunction caused by an excessive systemic inflammatory response to infection. Therefore, identifying negative regulators innate inflammation is crucial for treating this condition. In study, we aimed understand how transducin-like enhancer split 3 (TLE3) regulates responses. We detected Tle3 changes in sepsis patients analyzing public databases, which were confirmed septic survivors, mouse models, and macrophages using Western blotting,...

10.1016/j.jare.2025.03.041 article EN cc-by-nc-nd Journal of Advanced Research 2025-03-01

Toll-like receptor 4 (TLR4) has been implicated in the progression of cardiovascular disease, including hypertension. However, role TLR4 development prehypertension is uncertain.Prehypertensive rats were treated with 8% salt for 12 weeks to induce prehypertension. These then given either TAK-242 selective blocker, or vehicle by bilateral micro-injection paraventricular nucleus (PVN). Blood pressure (BP) and renal sympathetic nerve activity recorded. PVN expression TLR4, myeloid...

10.1093/ajh/hpy074 article EN American Journal of Hypertension 2018-05-02

Abstract Abnormal aggregation of pathological tau protein is a neuropathological feature Alzheimer’s disease (AD). In the AD patients, abnormal accumulation first appeared in entorhinal cortex (EC) and then propagated to hippocampus with microglia activation inflammation, but mechanism elusive. Here, we studied role mechanisms underlying periphery inflammation on brain transmission. By intraperitoneal injection lipopolysaccharide (LPS) medial (MEC)-specific overexpressing P301L human...

10.1042/bsr20193629 article EN Bioscience Reports 2020-02-01

Adipogenesis is closely related to various metabolic diseases, such as obesity, type 2 diabetes, cardiovascular diseases and cancer. This cellular process highly dependent on the expression sequential activation of a diverse group transcription factors. Here, we report that ADAR1 (also known ADAR) could inhibit adipogenesis through binding with Dicer DICER1), resulting in enhanced production miR-155-5p, which downregulates adipogenic early factor C/EBPβ. Consequently, levels late-stage...

10.1242/jcs.259333 article EN Journal of Cell Science 2022-01-24

Obesity is a global health threat, and the induction of white adipose tissue (WAT) browning presents promising therapeutic method for it. Recent publications revealed essential role protein arginine methyltransferase 4 (PRMT4) in lipid metabolism adipogenesis, but its involvement WAT has not been investigated. Our initial studies found that expression PRMT4 adipocytes was upregulated cold-induced downregulated obesity. Besides, overexpression inguinal accelerated thermogenesis to protect...

10.2337/db22-1016 article EN Diabetes 2023-05-22

Abstract In tauopathies, memory impairment positively strongly correlates with the amount of abnormal tau aggregates; however, how accumulation induces synapse is unclear. Recently, we found that human activated Signal Transduction and Activator Transcription-1 (STAT1) to inhibit transcription synaptic N-methyl-D-aspartate receptors (NMDARs). Here, overexpressing P301L mutant (P301L-hTau) increased phosphorylated level Transcription-3 (STAT3) at Tyr705 by JAK2, which would promote STAT3...

10.1038/s41392-020-00290-9 article EN cc-by Signal Transduction and Targeted Therapy 2020-12-26

Abstract Background Dysregulation of vascular homeostasis can induce cardiovascular diseases and increase global mortality rates. Although lineage tracing studies have confirmed the pivotal role modulated smooth muscle cells (VSMCs) in progression pathological remodeling, underlying mechanisms are still unclear. Methods The expression Tudor-SN was determined VSMCs artery stenosis, PDGF-BB-treated atherosclerotic plaque. Loss- gain-of-function approaches were used to explore modulation...

10.1186/s12929-024-01076-9 article EN cc-by Journal of Biomedical Science 2024-09-05

Cell migration is central to development and post-traumatic regeneration. The differential increase in 6-sulphated chondroitins during axonal growth both crushed sciatic nerves brain suggests that chondroitin 6-sulphotransferase-1 (C6ST-1) a key enzyme mediates cell the process. We have cloned cDNA of C6ST-1 gene (C6st1) (GenBank accession number AF178689) from adult rats produced ribonucleotide probes accordingly track signs at site injury. found C6st1 mRNA expression Schwann cells...

10.1242/jcs.02796 article EN Journal of Cell Science 2006-02-22

The association of 17β-hydroxysteroid dehydrogenase 10 (HSD10) with β-amyloid in the brain is known to contribute progression Alzheimer's disease. Further, it has been shown that interaction between purified HSD10 and inhibits its enzymatic activity. However, date no system developed enable study activity intact living cells. To address this significant shortcoming, we have a novel fluorogenic probe, (-)-cyclohexenyl amino naphthalene alcohol [(-)-CHANA], observe measure oxidation (-)-CHANA...

10.1021/cb100199m article EN ACS Chemical Biology 2010-09-13

There is accumulating evidence that decreased histone acetylation involved in normal aging and neurodegenerative diseases. Recently, we found ANP32A, a key component of INHAT (inhibitor acetyltransferases) suppresses acetylation, increased aged cognitively impaired C5 7 mice expressing wild-type human full length tau (htau) transgenic mice. Downregulating ANP32A restored cognitive function synaptic plasticity through upregulation the expressions synaptic-related proteins via increasing...

10.3233/jad-180090 article EN Journal of Alzheimer s Disease 2018-05-18
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