A5011815714- Cardiac Fibrosis and Remodeling
- Signaling Pathways in Disease
- Protease and Inhibitor Mechanisms
- Peptidase Inhibition and Analysis
- Immune cells in cancer
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Tissue Engineering and Regenerative Medicine
- Atherosclerosis and Cardiovascular Diseases
- Extracellular vesicles in disease
- Adipokines, Inflammation, and Metabolic Diseases
- Cardiovascular Function and Risk Factors
- Macrophage Migration Inhibitory Factor
- Cell Adhesion Molecules Research
- Cardiac Structural Anomalies and Repair
- Crystallization and Solubility Studies
- Quinazolinone synthesis and applications
- X-ray Diffraction in Crystallography
- Glycosylation and Glycoproteins Research
- Advanced Proteomics Techniques and Applications
- Phagocytosis and Immune Regulation
- Phenothiazines and Benzothiazines Synthesis and Activities
- Autophagy in Disease and Therapy
- Barrier Structure and Function Studies
- Acute Kidney Injury Research
- Immune Response and Inflammation
University of South Florida
2019-2025
Wuhan University
2016-2025
James A. Haley Veterans' Hospital
2025
Renmin Hospital of Wuhan University
2016-2025
Yangzhou University
2022-2024
Ministry of Education of the People's Republic of China
2023
Taizhou Vocational and Technical College
2017-2023
Second Hospital of Nanchang
2020
University of Mississippi Medical Center
2013-2019
Jackson Memorial Hospital
2013-2019
Abstract Pulmonary fibrosis is the pathologic basis for a variety of incurable human chronic lung diseases. IL-17A, glycoprotein secreted from IL-17–producing cells, has recently been shown to be proinflammatory cytokine involved in inflammation and autoimmune disease. In this study, we report that IL-17A increased synthesis secretion collagen promoted epithelial–mesenchymal transition alveolar epithelial cells TGF-β1–dependent manner. Using vivo fibrotic models, found expression elevated...
Although macrophage phenotypes have been well studied in the myocardial infarction (MI) setting, this study investigated temporal neutrophil polarization and activation mechanisms. Neutrophils isolated from infarcted left ventricle (LV) of mice showed high expression proinflammatory markers at Day 1 anti-inflammatory Days 5 7 post-MI, indicating distinct along post-MI time continuum. Flow cytometry analysis revealed that although N1 neutrophils were always predominant (>80% total each...
In response to myocardial infarction (MI), cardiac macrophages regulate inflammation and scar formation. We hypothesized that undergo polarization state changes over the MI time course assessed macrophage transcriptomic signatures first week of MI. C57BL/6 J male mice (3–6 months old) were subjected permanent coronary artery ligation induce MI, isolated from infarct region at days 1, 3, 7 post-MI. Day 0, no resident served as negative control. Whole transcriptome analysis was performed using...
Rationale: Matrix metalloproteinase (MMP)-28 regulates the inflammatory and extracellular matrix responses in cardiac aging, but roles of MMP-28 after myocardial infarction (MI) have not been explored. Objective: To determine impact deletion on post-MI remodeling left ventricle (LV). Methods Results: Adult C57BL/6J wild-type (n=76) MMP null (MMP-28 −/− , n=86) mice both sexes were subjected to permanent coronary artery ligation create MI. expression decreased post-MI, its cell source shifted...
Polymorphonuclear granulocytes (PMNs; neutrophils) serve as key effector cells in the innate immune system and provide first line of defense against invading microorganisms. In addition to producing inflammatory cytokines chemokines undergoing a respiratory burst that stimulates release reactive oxygen species, PMNs also degranulate components kill pathogens. Recently, neutrophil extracellular traps have been shown be an alternative way trap microorganisms contain infection. PMN-derived...
Cardiac fibroblasts are the major producers of extracellular matrix (ECM) to form infarct scar. We hypothesized that undergo a spectrum phenotype states over course myocardial infarction (MI) from early onset scar formation. Fibroblasts were isolated region C57BL/6J male mice (3–6 months old, n = 60) at days 0 (no MI control) and 1, 3, or 7 after MI. Whole transcriptome analysis was performed by RNA-sequencing. Of genes sequenced, 3371 differentially expressed Enrichment revealed day 1...
Abstract In response to myocardial infarction (MI), neutrophils (PMNs) are early responders that initiate the inflammatory reaction. Because macrophages and fibroblasts show polarization states after MI, we hypothesized PMNs also undergo phenotypic changes over MI time course. The objective of current study was map continuum phenotypes in cardiac first week MI. C57BL/6J male mice (3–6 months old) underwent permanent coronary artery ligation induce were isolated from infarct region at days 1,...
Sex differences in heart failure development following myocardial infarction (MI) are not fully understood. We hypothesized that differential MI signaling could explain variations outcomes. Analysis of the mouse attack research tool 1.0 (422 mice; young = 5.4 ± 0.1; old 23.3 0.1 months age) was used to dissect pathways, which validated a new cohort mice (4.8 0.2 age); and substantiated humans. Plasma collected at visit 2 from subset Jackson Heart Study (JHS; community-based study consisting...
Cardiac ageing involves the progressive development of cardiac fibrosis and diastolic dysfunction coordinated by MMP-9. Here, we report a signature that encompasses macrophage pro-inflammatory signalling in left ventricle (LV) distinguishes biological from chronological ageing. Young (6–9 months), middle-aged (12–15 old (18–24 senescent (26–34 months) mice both C57BL/6J wild type (WT) MMP-9 null were evaluated. Using an identified inflammatory pattern, able to define individual based on...
Severe lung infection can lead to brain dysfunction and neurobehavioral disorders. The mechanisms that regulate the lung-brain axis of inflammatory response respiratory are incompletely understood. This study examined effects causing systemic neuroinflammation as a potential mechanism contributing blood-brain barrier (BBB) leakage behavioral impairment.Lung in mice was induced by instilling Pseudomonas aeruginosa (PA) intratracheally. We determined bacterial colonization tissue,...
Abstract Cellular senescence contributes to inflammation and organ dysfunction during aging. While this process is generally characterized by irreversible cell cycle arrest, its morphological features functional impacts vary in different cells from various organs. In study, we examined the expression of multiple senescent markers lungs young aged humans mice, as well mouse lung endothelial cultured with a inducer, suberoylanilide hydroxamic acid (SAHA), or doxorubicin (DOXO). We detected...
Recent evidence indicates that toll-like receptor (TLR) 2 and 4 are involved in the pathogenesis of dilated cardiomyopathy (DCM), but exact mechanisms their actions have not been elucidated. We explored therapeutic potential blocking TLRs mice with established cardiomyopathy. Cardiomyopathy was generated by a single intraperitoneal injection doxorubicin (10 mg/kg). Two weeks later, were treated TLR2 or TLR4 neutralizing antibody. Blocking TLR2, TLR4, activity only reduced mortality, also...
Abstract Background About 6 million Americans suffer from heart failure and 70% of cases are caused by myocardial infarction (MI). Following infarction, increased cytokines induce two major types macrophages: classically activated macrophages which contribute to extracellular matrix destruction alternatively construction. Though experimental results have shown the transitions between these macrophages, little is known about dynamic progression activation. Therefore, objective this study...
Background— After myocardial infarction, the left ventricle undergoes a wound healing response that includes robust infiltration of neutrophils and macrophages to facilitate removal dead myocytes as well turnover extracellular matrix. Matrix metalloproteinase (MMP)-9 is key enzyme regulates post-myocardial infarction ventricular remodeling. Methods Results— Infarct regions from wild-type MMP-9 null mice (n=8 per group) analyzed by glycoproteomics showed 541 N -glycosylated proteins...