Yingying Le

ORCID: 0000-0002-7990-3899
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About
Contact & Profiles
Research Areas
  • S100 Proteins and Annexins
  • Immune Response and Inflammation
  • Antimicrobial Peptides and Activities
  • Chemokine receptors and signaling
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Immunotherapy and Immune Responses
  • Alzheimer's disease research and treatments
  • Wound Healing and Treatments
  • Pancreatic function and diabetes
  • Peptidase Inhibition and Analysis
  • Adipose Tissue and Metabolism
  • Computational Drug Discovery Methods
  • 3D Printing in Biomedical Research
  • HIV Research and Treatment
  • Bone Metabolism and Diseases
  • MicroRNA in disease regulation
  • Protease and Inhibitor Mechanisms
  • Cancer, Stress, Anesthesia, and Immune Response
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • interferon and immune responses
  • Pancreatitis Pathology and Treatment
  • Neuropeptides and Animal Physiology
  • Wnt/β-catenin signaling in development and cancer
  • Adipokines, Inflammation, and Metabolic Diseases
  • Sirtuins and Resveratrol in Medicine

Jilin University
2025

University of Chinese Academy of Sciences
2012-2024

Shanghai Institute of Nutrition and Health
2019-2024

Ruihua Affiliated Hospital of Soochow University
2017-2024

China Southern Power Grid (China)
2024

Soochow University
2017-2024

Deleted Institution
2016-2022

Shanghai Institutes for Biological Sciences
2011-2020

Yangzhou University
2020

Chinese Academy of Sciences
2010-2019

Amyloid ␤ (A␤) is a major contributor to the pathogenesis of Alzheimer's disease (AD).Although A␤ has been reported be directly neurotoxic, it also causes indirect neuronal damage by activating mononuclear phagocytes (microglia) that accumulate in and around senile plaques.In this study, we show 42 amino acid form amyloid peptide, , chemotactic agonist for seven-transmembrane, G-protein-coupled receptor named FPR-Like-1 (FPRL1), which expressed on human phagocytes.Moreover, FPRL1 at high...

10.1523/jneurosci.21-02-j0003.2001 article EN cc-by-nc-sa Journal of Neuroscience 2001-01-15

Abstract Alzheimer’s disease (AD) is characterized by overproduction of β amyloid peptides in the brain with progressive loss neuronal cells. The 42-aa form peptide (Aβ42) implied as a major causative factor, because it toxic to neurons and elicits inflammatory responses activating microglial Despite Aβ42, AD tissue also generates protective factor(s) that may antagonize neurodestructive effect Aβ42. Humanin gene cloned from an apparently normal region encodes 24-aa peptide. Both secreted...

10.4049/jimmunol.172.11.7078 article EN The Journal of Immunology 2004-06-01

Abstract Background Inflammatory responses in the CNS mediated by activated glial cells play an important role host-defense but are also involved development of neurodegenerative diseases. Resveratrol is a natural polyphenolic compound that has cardioprotective, anticancer and anti-inflammatory properties. We investigated capacity resveratrol to protect microglia astrocyte from inflammatory insults explored mechanisms underlying different inhibitory effects on astrocytes. Methods A murine...

10.1186/1742-2094-7-46 article EN cc-by Journal of Neuroinflammation 2010-08-17

Alzheimers disease (AD) is characterized by amyloid plaques and neurofibrillary tangles associated with chronic inflammation. APPswe/PS1dE9 an AD mouse model bearing mutant transgenes of precursor protein presenilin-1. Amyloid deposition present in this at early stage life. However, the progression inflammation its relationship have not been characterized. Here we showed that were 4 months age increased age. CD11b-positive microglia clusters appeared hippocampus neocortex Clustered glial...

10.2174/156720509790147070 article EN Current Alzheimer Research 2009-12-01

The endoplasmic reticulum quality control protein activating transcription factor 6 (ATF6) has emerged as a novel metabolic regulator. Here, we show that adenovirus-mediated overexpression of the dominant-negative form ATF6 (dnATF6) increases susceptibility to develop hepatic steatosis in diet-induced insulin-resistant mice and fasted mice. Overexpression dnATF6 or small interfering RNA-mediated knockdown decreases transcriptional activity peroxisome proliferator-activated receptor α...

10.2337/db15-1637 article EN Diabetes 2016-04-12

Identifying functional enzymes for the catalysis of specific biochemical reactions is a major bottleneck in de novo design biosynthesis and biodegradation pathways. Conventional methods based on microbial screening metagenomics require long verification periods incur high experimental costs; recent data-driven apply only to few common substrates. To enable rapid high-throughput identification complex less-studied substrates, we propose robust enzyme's substrate promiscuity prediction model...

10.1021/acscatal.3c04461 article EN ACS Catalysis 2024-02-16

Trp-Lys-Tyr-Val-D-Met (WKYMVm) is a synthetic leukocyte-activating peptide postulated to use seven-transmembrane, G protein-coupled receptor(s). In the study characterize receptor(s) for WKYMVm, we found that this induced marked chemotaxis and calcium flux in human phagocytes. The signaling by WKYMVm phagocytes was attenuated high concentrations of bacterial chemotactic fMLP, suggesting might fMLP. This hypothesis tested using cells over expressing genes encoding two seven-transmembrane...

10.4049/jimmunol.163.12.6777 article EN The Journal of Immunology 1999-12-15

The 42 amino acid form of beta amyloid (Abeta42) plays a pivotal role in neurotoxicity and the activation mononuclear phagocytes Alzheimer's disease (AD). Our recent study revealed that FPRL1, G-protein-coupled receptor, mediates chemotactic activating effect Abeta42 on (monocytes microglia), suggesting FPRL1 may be involved proinflammatory responses AD. We investigated cellular uptake subsequent fibrillar formation by using fluorescence confocal microscopy. found upon incubation with...

10.1096/fj.01-0251com article EN The FASEB Journal 2001-11-01

Abstract Prion diseases are transmissible and fatal neurodegenerative disorders which involve infiltration activation of mononuclear phagocytes at the brain lesions. A 20-aa acid fragment human cellular prion protein, PrP106–126, was reported to mimic biological activity pathologic isoform activates phagocytes. The cell surface receptor(s) mediating PrP106–126 is unknown. In this study, we show that chemotactic for monocytes through use a G protein-coupled receptor formyl peptide...

10.4049/jimmunol.166.3.1448 article EN The Journal of Immunology 2001-02-01

The formylpeptide receptor (FPR) is a G-protein-coupled (GPCR) that mediates chemotaxis of phagocytic leukocytes induced by bacterial peptide N-formyl-methionyl-leucyl-phenylalanine (fMLF). We previously showed selected human glioma cell lines also express functional FPR. therefore investigated the relationship between FPR expression and biologic behavior cells.Expression function in glioblastoma line U-87 were examined reverse transcription-polymerase chain reaction (RT-PCR) assays,...

10.1093/jnci/dji142 article EN JNCI Journal of the National Cancer Institute 2005-05-31

Locus ceruleus (LC) is the main subcortical site of norepinephrine synthesis. In Alzheimer's disease (AD) patients and rodent models, degeneration LC neurons reduced levels in projection areas are significantly correlated with increase amyloid plaques, neurofibrillary tangles, severity dementia. Activated microglia play a pivotal role progression AD by either clearing β peptide (Aβ) deposits through uptake Aβ or releasing cytotoxic substances proinflammatory cytokines. Here, we investigated...

10.1523/jneurosci.2985-10.2010 article EN cc-by-nc-sa Journal of Neuroscience 2010-09-01

Abstract The formylpeptide receptor-like 1, now officially termed FPR2, in human and its mouse homolog mFPR2 mediate leukocyte migration response to agonists associated with inflammation immune responses. To clarify the vivo role of receptor, we generated mice deficient mFPR2. mFPR2−/− showed markedly reduced severity OVA/alum-induced allergic airway inflammation. This was diminished recruitment CD11c+ dendritic cells into mucosa secondary lymphoid organs, as well production Type 2 cytokines...

10.4049/jimmunol.0903022 article EN The Journal of Immunology 2010-03-04

Commensal bacteria and their products provide beneficial effects to the mammalian gut by stimulating epithelial cell turnover enhancing wound healing, without activating overt inflammation. We hypothesized that N-formylpeptide receptors, which bind bacterial N-formylpeptides are expressed intestinal cells, may contribute these processes. Here we report formylpeptide receptor-2 (FPR2), show is on apical lateral membranes of colonic crypt mediates N-formylpeptide–dependent proliferation...

10.1172/jci65569 article EN Journal of Clinical Investigation 2013-03-01

Summary Introduction Hyperglycemia‐induced oxidative stress has been implicated in diabetic vascular complications which NADPH oxidase is a major source of reactive oxygen species ( ROS ) generation. Resveratrol naturally occurring polyphenol, vasoprotective effects animal models and inhibits high glucose HG )–induced endothelial cells. Aims We aimed to examine whether ‐induced activation production contribute glucotoxicity cells the effect resveratrol on glucotoxicity. Results Using murine...

10.1111/cns.12131 article EN other-oa CNS Neuroscience & Therapeutics 2013-06-03

Amyloid-β (Aβ), a natural product of cell metabolism, plays key role in the pathogenesis Alzheimer's disease (AD). Epidemiological studies indicate patients with AD have an increased risk developing type 2 diabetes mellitus (T2DM). Aβ can induce insulin resistance cultured hepatocytes by activating JAK2/STAT3/SOCS-1 signaling pathway. Amyloid precursor protein and presenilin 1 double-transgenic mouse models circulating level show impaired glucose/insulin tolerance hepatic resistance....

10.2337/db12-0670 article EN cc-by-nc-nd Diabetes 2012-12-07

Wound healing is a multi-phased pathophysiological process requiring chemoattractant receptor-dependent accumulation of myeloid cells in the lesion. Two G protein-coupled formylpeptide receptors Fpr1 and Fpr2 mediate rapid neutrophil infiltration liver Listeria-infected mice by sensing pathogen-derived chemotactic ligands. These also recognize host-derived peptides inflammation injury. Here we report capacity Fprs to promote sterile skin wound initiating infiltration. We found that normal...

10.1371/journal.pone.0090613 article EN cc-by PLoS ONE 2014-03-06

Obesity and related inflammation are critical for the pathogenesis of insulin resistance, but underlying mechanisms not fully understood. Formyl peptide receptor 2 (FPR2) plays important roles in host immune responses inflammation-related diseases. We found that Fpr2 expression was elevated white adipose tissue high-fat diet (HFD)–induced obese mice db/db mice. The systemic deletion alleviated HFD-induced obesity, hyperglycemia, hyperlipidemia, hepatic steatosis. Furthermore, HFD-fed body...

10.2337/db18-0469 article EN Diabetes 2019-03-12

Abstract Receptors for the bacterial chemotactic peptide fMLP are implicated in inflammation and host defense against microbial infection. We investigated expression function of fMLPR microglial cells, which share characteristics mononuclear phagocytes play an important role proinflammatory responses CNS. The genes encoding formyl receptor (FPR)1 FPR2, high- low-affinity fMLPR, was detected a murine cell line N9, but these cells did not respond to agonists known receptors. N9 incubated with...

10.4049/jimmunol.168.1.434 article EN The Journal of Immunology 2002-01-01

Background Under stress, AMP-activated protein kinase (AMPK) plays a central role in energy balance, and the heat shock response is protective mechanism for cell survival. The relationship between AMPK activity (HSP) expression under stress unclear. Methodology/Principal Findings We found that induced dephosphorylation of AMPKα subunit (AMPKα) various types from human rodent. In HepG2 cells, turn caused acetyl-CoA carboxylase upregulation phosphoenolpyruvate carboxykinase, two downstream...

10.1371/journal.pone.0013096 article EN cc-by PLoS ONE 2010-10-01
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