A5061247919- Hepatitis C virus research
- Atherosclerosis and Cardiovascular Diseases
- Peroxisome Proliferator-Activated Receptors
- Immune Response and Inflammation
- Cholesterol and Lipid Metabolism
- Glaucoma and retinal disorders
- Mitochondrial Function and Pathology
- Immune cells in cancer
- Hepatitis B Virus Studies
- interferon and immune responses
- Lipoproteins and Cardiovascular Health
- Retinal Diseases and Treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Sphingolipid Metabolism and Signaling
- Immune Cell Function and Interaction
- Antioxidant Activity and Oxidative Stress
- Lipid metabolism and biosynthesis
- Alzheimer's disease research and treatments
- Technology and Data Analysis
- HIV Research and Treatment
- Monoclonal and Polyclonal Antibodies Research
- Cancer-related gene regulation
- Liver Disease Diagnosis and Treatment
- Ubiquitin and proteasome pathways
- NF-κB Signaling Pathways
University of California, San Diego
2013-2024
La Jolla Alcohol Research
2015
Hallym University
2001-2009
Rationale : Oxidized low-density lipoprotein (LDL) is an important determinant of inflammation in atherosclerotic lesions. It has also been documented that certain chronic infectious diseases, such as periodontitis and chlamydial infection, exacerbate clinical manifestations atherosclerosis. In addition, low-level but persistent metabolic endotoxemia often found diabetic obese subjects induced mice fed a high-fat diet. Objective this study, we examined cooperative macrophage activation by...
Neuroinflammation is a major component in the transition to and perpetuation of neuropathic pain states. Spinal neuroinflammation involves activation TLR4, localized enlarged, cholesterol-enriched lipid rafts, designated here as inflammarafts. Conditional deletion cholesterol transporters ABCA1 ABCG1 microglia, leading inflammaraft formation, induced tactile allodynia naive mice. The apoA-I binding protein (AIBP) facilitated depletion from inflammarafts reversed model chemotherapy-induced...
Lipoprotein oxidation plays an important role in pathogenesis of atherosclerosis. Oxidized low density lipoprotein (OxLDL) induces profound inflammatory responses vascular cells, such as production monocyte chemoattractant protein-1 (MCP-1) [chemokine (C-C motif) ligand 2], a key chemokine the initiation and progression inflammation. Here we demonstrate that OxLDL also binds MCP-1 OxLDL-bound retains its ability to recruit monocytes. A human mutant which basic amino acids Arg-18 Lys-19 were...
Adaptive immunity, which plays an important role in the development of atherosclerosis, is mediated by major histocompatibility complex (MHC)-dependent antigen presentation. In atherosclerotic lesions, macrophages constitute class antigen-presenting cells that activate adaptive immune responses to oxidized low-density lipoprotein (OxLDL). It has been reported autophagy regulates enhancing presentation MHC II (MHC-II). a previous study, we have demonstrated SYK (spleen tyrosine kinase)...
Transforming growth factor-β (TGF-β) is implicated in the pathogenesis of liver disease. TGF-β involved both regeneration and fibrotic cirrhotic transformation with hepatitis viral infection. Hepatitis C virus (HCV) infection often leads to cirrhosis hepatocellular carcinoma. HCV nonstructural 5A (NS5A) protein a multifunctional that modulates cytokine-mediated signal transduction pathways. To elucidate molecular mechanism pathogenesis, we examined effect NS5A on TGF-β-stimulated signaling...
Hepatitis C virus (HCV) is a major cause of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC). However, the mechanism HCV pathogenesis not well understood. Our previous in vitro studies suggested that non-structural 5A (NS5A) protein may play an important role pathogenesis. To elucidate HCV-induced pathogenesis, we investigated histopathological changes transgenic mice harbouring NS5A gene. We generated gene under control hepatitis B (HBV) enhancer. Pathological were...
Oxidation of low-density lipoprotein (LDL) is one the major causative mechanisms in development atherosclerosis. In previous studies, we showed that minimally oxidized LDL (mmLDL) induced inflammatory responses macrophages, macropinocytosis and intracellular lipid accumulation cholesterol esters (OxCEs) were biologically active components mmLDL. Here identified a specific OxCE molecule responsible for biological activity mmLDL characterized signaling pathways macrophages response to this...
Apolipoprotein A-I binding protein (AIBP) has been shown to augment cholesterol efflux from endothelial cells and macrophages. In zebrafish mice, AIBP-mediated regulation of levels in the plasma membrane controls angiogenesis. The goal this work was evaluate metabolic changes atherosclerosis AIBP loss-of-function gain-of-function animal studies. Here, we show that Apoa1bp−/−Ldlr−/− mice fed a high-cholesterol, high-fat diet had exacerbated weight gain, liver steatosis, glucose intolerance,...
Acute respiratory distress syndrome (ARDS) is characterized by an excessive pulmonary inflammatory response. Removal of excess cholesterol from the plasma membrane cells helps reduce their activation. The secreted apolipoprotein A-I binding protein (AIBP) has been shown to augment efflux endothelial lipoprotein HDL. Here, we find that AIBP was expressed in human lung and into bronchoalveolar space mice subjected inhalation LPS. bound surfactant B increased alveolar macrophages calfactant, a...
Abstract Impairment of mitochondrial structure and function is strongly linked to glaucoma pathogenesis. Despite the widely appreciated disease relevance dysfunction loss, molecular mechanisms underlying fragmentation metabolic stress in are poorly understood. We demonstrate here that glaucomatous retinal ganglion cells (RGCs) show loss A-kinase anchoring protein 1 (AKAP1), activation calcineurin (CaN) reduction dynamin-related (Drp1) phosphorylation at serine 637 (Ser637). These findings...
Apolipoprotein A-I binding protein (AIBP) is a recently identified innate anti-inflammatory factor. Here, we show that AIBP inhibited HIV replication by targeting lipid rafts and reducing virus-cell fusion. Importantly, selectively reduced levels of on cells stimulated an inflammatory stimulus or treated with extracellular vesicles containing HIV-1 Nef without affecting nonactivated cells. Accordingly, fusion monocyte-derived macrophages was sensitive to only in the presence Nef. Silencing...
Glaucoma is a leading cause of blindness worldwide in individuals 60 years age and older. Despite its high prevalence, the factors contributing to glaucoma progression are currently not well characterized. Glia-driven neuroinflammation mitochondrial dysfunction play critical roles glaucomatous neurodegeneration. Here, we demonstrated that elevated intraocular pressure (IOP) significantly decreased apolipoprotein A-I binding protein (AIBP; gene name Apoa1bp) retinal ganglion cells (RGCs), but...
The nonstructural 5A (NS5A) protein of hepatitis C virus (HCV) is a phosphoprotein possessing various functions. We have previously reported that the HCV NS5A interacts with tumor necrosis factor (TNF) receptor-associated (TRAF) domain TRAF2 (Park, K.-J., Choi, S.-H., Lee, S. Y., Hwang, B., and Lai, M. C. (2002) J. Biol. Chem. 277, 13122–13128). Both TNF-α- TRAF2-mediated nuclear factor-κB (NF-κB) activations were inhibited by NS5A-TRAF2 interaction. Because required for activation both...
Objective: Atherosclerotic lesions are often characterized by accumulation of OxLDL (oxidized low-density lipoprotein), which is associated with vascular inflammation and lesion vulnerability to rupture. Extracellular AIBP (apolipoprotein A-I binding protein; encoded APOA1BP gene), when secreted, promotes cholesterol efflux regulates lipid rafts dynamics, but its role as an intracellular protein in mammalian cells remains unknown. The aim this work was determine the function macrophages...
Oxidative modification of low-density lipoprotein (LDL) turns it into an endogenous ligand recognized by pattern-recognition receptors. We have demonstrated that minimally oxidized LDL (mmLDL) binds to CD14 and mediates TLR4/MD-2-dependent responses in macrophages, many which are MyD88-independent. also the mmLDL activation leads recruitment spleen tyrosine kinase (Syk) TLR4 Syk phosphorylation. In this study, we produced a macrophage-specific knockout mouse used primary Syk(-/-) macrophages...
Microglia-driven neuroinflammation plays an important role in the development of Alzheimer's disease. Microglia activation is accompanied by formation and chronic expression TLR4 inflammarafts, defined as enlarged cholesterol-rich lipid rafts serving assembly platform for dimers complexes other inflammatory receptors. The secreted apoA-I binding protein (APOA1BP or AIBP) binds selectively targets cholesterol depletion machinery to inflammaraft-expressing inflammatory, but not homeostatic...
Reprogramming of monocytes and macrophage manifests in hyperinflammatory responses chronification inflammation atherosclerosis. Recent studies focused on epigenetic, transcriptional, metabolic alterations that characterize trained immunity. However, the underlying effector mechanisms driving response reprogrammed macrophages remain unclear. We hypothesized plasma membrane atherosclerotic lesion undergoes reprogramming to maintain inflammarafts, enlarged lipid rafts (LR) serving as a platform...
AIBP (apolipoprotein A-I binding protein) is an effective and selective regulator of lipid rafts modulating many metabolic pathways originating from the rafts, including inflammation. The mechanism action was suggested to involve stimulation by cholesterol efflux, depleting cholesterol, which essential for raft integrity. Here we describe a different contributing regulation AIBP. Approach Results: We demonstrate that modulation may not exclusively depend on rate efflux or presence key ABCA1...