A5064921147- Cardiac Fibrosis and Remodeling
- Signaling Pathways in Disease
- Peptidase Inhibition and Analysis
- Protease and Inhibitor Mechanisms
- Muscle Physiology and Disorders
- Cardiomyopathy and Myosin Studies
- Immune cells in cancer
- Cardiovascular Effects of Exercise
- Phagocytosis and Immune Regulation
- Cardiovascular Disease and Adiposity
- Angiogenesis and VEGF in Cancer
- Glycosylation and Glycoproteins Research
- Clusterin in disease pathology
- Oral microbiology and periodontitis research
- Sepsis Diagnosis and Treatment
- Biomarkers in Disease Mechanisms
- Advanced Proteomics Techniques and Applications
- Neuropeptides and Animal Physiology
- Nerve injury and regeneration
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Atherosclerosis and Cardiovascular Diseases
- Macrophage Migration Inhibitory Factor
- Transcranial Magnetic Stimulation Studies
- Viral Infectious Diseases and Gene Expression in Insects
- Receptor Mechanisms and Signaling
Vanderbilt University Medical Center
2020-2024
Sarah Cannon
2019
University of Mississippi Medical Center
2014-2018
Jackson Memorial Hospital
2014-2018
The University of Texas Health Science Center at San Antonio
2015
Johns Hopkins University
2015
University of Alabama at Birmingham
2015
G.V. (Sonny) Montgomery VA Medical Center
2015
Johns Hopkins Medicine
2015
The University of Texas at San Antonio
2015
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...
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...
Chronic inflammatory diseases, such as periodontal disease, associate with adverse wound healing in response to myocardial infarction (MI). The goal of this study was elucidate the molecular basis for impaired cardiac setting periodontal-induced chronic inflammation. Causal network analysis 168 and extracellular matrix genes revealed that inflammation induced by a subseptic dose Porphyromonas gingivalis lipopolysaccharide (LPS) exacerbated infarct expression proinflammatory cytokine Ccl12....
Advancing age is an independent risk factor for cardiovascular disease. Matrix metalloproteinase-9 (MMP-9) secreted by macrophages and robustly increases in the left ventricle (LV) with age. The present study investigated effect of MMP-9 overexpression on cardiac aging. We compared 16- to 21-mo-old C57BL/6J wild-type (WT) transgenic (TG) male female mice (n = 15-20/group). amplified hypertrophic response aging, as evidenced increased LV wall thickness myocyte cross-sectional areas (P < 0.05...
Objective: Sepsis remains a predominant cause of mortality in the ICU, yet strategies to increase survival have proved largely unsuccessful. This study aimed identify proteins linked sepsis outcomes using glycoproteomic approach target extracellular that trigger downstream pathways and direct patient outcomes. Design: Plasma was obtained from Lactate Assessment Treatment Early cohort. N-linked plasma glycopeptides were quantified by solid-phase extraction coupled with mass spectrometry....
Macrophage phagocytosis of dead cells is a prerequisite for inflammation resolution. Because CXCL4 induces macrophage in vitro, we examined the impact exogenous infusion on cardiac wound healing and following myocardial infarction (MI).CXCL4 expression significantly increased infarct region beginning at Day 3 post-MI, macrophages were predominant source. Adult male C57BL/6J mice subjected to coronary artery occlusion, MI randomly infused with recombinant mouse or saline 24 h post-MI by...
Abstract Endothelial cells (ECs) have essential roles in cardiac tissue repair after myocardial infarction (MI). To establish stage-specific and long-term effects of the ischemic injury on ECs, we analyzed their transcriptome at landmark time points MI mice. We found that early EC response Day 2 post-MI centered metabolic changes, acquisition proinflammatory phenotypes, initiation S phase cell cycle, activation stress-response pathways, followed by progression to mitosis (M/G2 phase)...
The purpose of this study was to evaluate the effect sham surgery in a minimally invasive surgical model permanent coronary artery occlusion used generate myocardial infarction (MI) mice. Adult male C57BL/6J mice (3-6 mo old) were divided into five groups: day (D) 0 (no operation), D1 Sham, MI, D7 and MI. A refined MI technique approach without ribs being cut. Both had left ventricle (LV) exposed through small incision. To test effects alone, suture passed around but not ligated. subjected...
Extracellular proteins are easily accessible, which presents a subproteome of molecular targets that have high diagnostic and therapeutic potential. Efforts been made to catalog the cardiac extracellular matridome analyze topology identified for design targets. Although many bioinformatics tools developed predict protein topology, has experimentally validated only very small portion membrane proteins. The aim this study was use glycoproteomics MS approach identify glycoproteins in infarcted...
The generation of big data has enabled systems-level dissections into the mechanisms cardiovascular pathology. Integration genetic, proteomic, and pathophysiological variables across platforms laboratories fosters discoveries through multidisciplinary investigations minimizes unnecessary redundancy in research efforts. Mouse Heart Attack Research Tool (mHART) consolidates a large set over 10 yr experiments from single laboratory for investigators to generate novel hypotheses identify new...
Brain-derived neurotrophic factor (BDNF) is a neuronal growth and survival that harbors cardioprotective qualities may attenuate dilated cardiomyopathy. In ~30% of the population, BDNF has common, nonsynonymous single nucleotide polymorphism rs6265 (Val66Met), which might be correlated with increased risk cardiovascular events. We previously showed correlates better cardiac function in Duchenne muscular dystrophy (DMD) patients. However, effect Val66Met on not been determined. The goal...
Pro‐inflammatory M1 and anti‐inflammatory M2 macrophages are involved in cardiac repair after myocardial infarction (MI). Mice with matrix metalloproteinase (MMP)‐28 deletion display decreased inflammation at day 7 post‐MI. Accordingly, we hypothesized that MMP‐28 polarizes to a pro‐inflammatory phenotype. In this study, stimulated peritoneal isolated from 3 6 month old male C57/BL6J mice recombinant protein evaluated cell By quantitative RT‐PCR, the catalytic domain only dose‐dependently...
Early inhibition of matrix metalloproteinase‐12 (MMP‐12) worsens cardiac remodeling post‐myocardial infarction (MI), suggesting a beneficial role for MMP‐12. This study assessed whether exogenous MMP‐12 delivery early post‐MI is an effective therapeutic approach. Male C57BL/6J mice (3–6 months old, n=3/group) were subjected to left coronary artery ligation. Saline or active (aMMP‐12; 0.5mg/kg/day) infusion was initiated at 3h using osmotic mini‐pump. Mice sacrificed day (d) 1 5 post‐MI. D0...
We previously identified brain-derived neurotrophic factor (BDNF) as a putative cardiac-specific biomarker for preserved cardiac function in Duchenne Muscular Dystrophy (DMD). BDNF has cardioprotective qualities that may attenuate dilated cardiomyopathy, and common, functional single nucleotide polymorphism rs6265 (Val66-Met) be correlated with increased risk of cardiovascular events. hypothesized is protective the setting DMD BDNF’s beneficial effects are diminished allelic carriers....