A5100663167- Immune cells in cancer
- Atherosclerosis and Cardiovascular Diseases
- Immune Cell Function and Interaction
- Cytokine Signaling Pathways and Interactions
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Immune Response and Inflammation
- Cancer-related molecular mechanisms research
- Inflammasome and immune disorders
- MicroRNA in disease regulation
- Diabetes and associated disorders
- NF-κB Signaling Pathways
- Diet and metabolism studies
- Mitochondrial Function and Pathology
- Liver Disease Diagnosis and Treatment
- RNA modifications and cancer
- Hippo pathway signaling and YAP/TAZ
- Renal and related cancers
- Folate and B Vitamins Research
- Peroxisome Proliferator-Activated Receptors
- Circular RNAs in diseases
- Adipokines, Inflammation, and Metabolic Diseases
- Aquaculture Nutrition and Growth
- Cell death mechanisms and regulation
- Ferroptosis and cancer prognosis
- Anxiety, Depression, Psychometrics, Treatment, Cognitive Processes
University of Pennsylvania
2017-2024
Chinese Academy of Fishery Sciences
2024
Ministry of Agriculture and Rural Affairs
2024
California Institute for Regenerative Medicine
2023-2024
Binzhou Medical University
2023-2024
Binzhou University
2023-2024
Shanghai Jiao Tong University
2010-2024
Changchun University of Science and Technology
2024
The Affiliated Yongchuan Hospital of Chongqing Medical University
2021-2024
Chongqing Medical University
2021-2024
It remains unknown whether newly identified anti-inflammatory/immunosuppressive cytokine interleukin-35 (IL-35) is different from other anti-inflammatory cytokines such as IL-10 and transforming growth factor (TGF)-β in terms of inhibition inflammation initiation suppression full-blown inflammation. Using experimental database mining statistical analysis methods we developed, examined the tissue expression profiles regulatory mechanisms IL-35 comparison to cytokines. Our results suggest that...
Hyperlipidemia-induced endothelial cell (EC) activation is considered as an initial event responsible for monocyte recruitment in atherogenesis. However, it remains poorly defined what the mechanism underlying hyperlipidemia-induced EC activation. Here, we tested a novel hypothesis that mitochondrial reactive oxygen species (mtROS) serve signaling mediators early atherosclerosis.Metabolomics and transcriptomics analyses revealed several lysophosphatidylcholine (LPC) species, such 16:0, 18:0,...
The role of receptors for endogenous metabolic danger signals-associated molecular patterns has been characterized recently as bridging innate immune sensory systems to initiation inflammation in bone marrow-derived cells, such macrophages. However, it remains unknown whether endothelial cells (ECs), the cell type with largest numbers and first vessel exposed circulating blood, can sense hyperlipidemia. This report determined caspase-1 plays a ECs sensing hyperlipidemia promoting EC...
Vascular response is an essential pathological mechanism underlying various inflammatory diseases. This study determines whether IL-35, a novel responsive anti-inflammatory cytokine, inhibits vascular in acute inflammation. Using mouse model of LPS-induced inflammation and plasma samples from sepsis patients, we found that IL-35 was induced the mice after LPS injection as well patients. In addition, decreased proinflammatory cytokines chemokines mice. Furthermore, inhibited leukocyte...
IL-35 (interleukin-35) is an anti-inflammatory cytokine, which inhibits immune responses by inducing regulatory T cells and B suppressing effector macrophages. It remains unknown whether atherogenic stimuli induce lipid-induced endothelial cell (EC) activation atherosclerosis. EC induced hyperlipidemia stimuli, including lysophosphatidylcholine considered as initiation step for monocyte recruitment In this study, we examined the expression of during early atherosclerosis roles mechanisms in...
Abstract Inflammation induced by lung infection is a double-edged sword, moderating both anti-viral and immune pathogenesis effects; the mechanism of latter not fully understood. Previous studies suggest vasculature involved in tissue injury. Here, we report that expression Sparcl1, secreted matricellular protein, upregulated pulmonary capillary endothelial cells (EC) during influenza-induced Endothelial overexpression SPARCL1 promotes detrimental inflammation, with inducing ‘M1-like’...
Deficient angiogenesis may contribute to worsen the prognosis of myocardial ischemia, peripheral arterial disease, ischemic stroke, etc. Dyslipidemic and inflammatory environments attenuate endothelial cell (EC) proliferation angiogenesis, worsening ischemia. Under these dyslipidemic environments, EC-caspase-1 becomes activated induces death that is defined as pyroptosis. However, underlying mechanism correlates caspase-1 activation with angiogenic impairment ischemia remains poorly defined....
Obesity paradox (OP) describes a widely observed clinical finding of improved cardiovascular fitness and survival in some overweight or obese patients. The molecular mechanisms underlying OP remain enigmatic partly due to lack animal models mirroring Using apolipoprotein E knock-out (apoE−/−) mice on high fat (HF) diet as an atherosclerotic obesity model, we demonstrated 1) microRNA-155 (miRNA-155, miR-155) is significantly up-regulated the aortas apoE−/− mice, miR-155 deficiency inhibits...
Uric Acid (UA), historically considered as a waste of cellular metabolism, has now received increasing attention because it was found to directly participate in the pathogenesis many human diseases including neurological disorders.On one hand, low levels UA are detrimental neurons its induction impairs antioxidant capacity cell.High UA, on other lead an inflammatory response contributing gout or neuroprotection.In this review, we summarize biphasic function uric acid and highlight potential...
It has been shown that anti-inflammatory cytokines interleukin-35 (IL-35) and IL-10 could inhibit acute endothelial cell (EC) activation, however, it remains unknown if by what pathways IL-35 block atherogenic lipid lysophosphatidylcholine (LPC)-induced sustained EC activation; mitochondrial reactive oxygen species (mtROS) can differentiate mediation of activation from trained immunity (innate immune memory). Using RNA sequencing analyses, biochemical assays, as well database mining...
To test our hypothesis that proatherogenic lysophosphatidylcholine (LPC) upregulates trained immunity pathways (TIPs) in human aortic endothelial cells (HAECs), we conducted an intensive analyses on RNA-Seq data and histone 3 lysine 14 acetylation (H3K14ac)-CHIP-Seq data, both performed HAEC treated with LPC. Our analysis revealed that: 1) LPC induces upregulation of three TIPs including glycolysis enzymes (GE), mevalonate (ME), acetyl-CoA generating (ACE); 2) 29% 31 acetyltransferases,...
Abstract Background Depression is a psychiatric disorder with global public health concerns. Although number of risk factors have been identified for depression, there no clear relationship between biochemistry and depression. In this study, we assessed whether depressive disorders are significantly associated biochemical indicators. Methods Our study included 17,561 adults (age ≥ 18 years) participating in the 2009-2018 National Health Nutrition Examination Survey (NHANES). The depression...
Macrophages are integral components of the innate immune system, playing a dual role in host defense during infection and pathophysiological states. contribute to responses aid combatting various infections, yet their production abundant proinflammatory cytokines can lead uncontrolled inflammation worsened tissue damage. Therefore, reducing macrophage-derived cytokine release represents promising approach for treating acute chronic inflammatory disorders. However, limited macrophage-specific...