A5069993102- Atherosclerosis and Cardiovascular Diseases
- Cell Adhesion Molecules Research
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Hippo pathway signaling and YAP/TAZ
- Cardiovascular Function and Risk Factors
- Eicosanoids and Hypertension Pharmacology
- Fatty Acid Research and Health
- Angiogenesis and VEGF in Cancer
- Inflammasome and immune disorders
- Immune cells in cancer
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- interferon and immune responses
- Protease and Inhibitor Mechanisms
- Ferroptosis and cancer prognosis
- Kruppel-like factors research
- Cancer, Hypoxia, and Metabolism
- Neonatal Health and Biochemistry
- Cardiac Valve Diseases and Treatments
- Heme Oxygenase-1 and Carbon Monoxide
- IL-33, ST2, and ILC Pathways
- NF-κB Signaling Pathways
- Cholesterol and Lipid Metabolism
- Nuclear Receptors and Signaling
- Axon Guidance and Neuronal Signaling
- Hemoglobin structure and function
Louisiana State University in Shreveport
2025
University of Nebraska Medical Center
2025
Louisiana State University Health Sciences Center Shreveport
2018-2024
University of Sheffield
2013-2024
Louisiana State University Health Sciences Center New Orleans
2024
Louisiana State University
2020-2021
The endothelium is critically involved in the pathogenesis of atherosclerosis by producing pro-inflammatory mediators, including IL-1β. Coronary arteries from patients with ischemic heart disease express large amounts IL-1β endothelium. However, mechanism which endothelial cells (ECs) release remains to be elucidated. We investigated neutrophil elastase (NE), a potent serine protease detected vulnerable areas human carotid plaques, as potential "trigger" for processing and release. This...
Objective- Alterations in extracellular matrix quantity and composition contribute to atherosclerosis, with remodeling of the subendothelial basement membrane an FN (fibronectin)-rich preceding lesion development. Endothelial cell interactions prime inflammatory responses a variety atherogenic stimuli; however, mechanisms regulating early accumulation remain unknown. We previously demonstrated that oxLDL (oxidized low-density lipoprotein) promotes endothelial proinflammatory gene expression...
Objective— Flow patterns differentially regulate endothelial cell phenotype, with laminar flow promoting vasodilation and disturbed proinflammatory activation. CSE (cystathionine γ-lyase), a major source of hydrogen sulfide (H 2 S) in cells, critically regulates cardiovascular function, by both reducing Therefore, we sought to investigate the role response flow. Approach Results— Wild-type C57Bl/6J knockout ( −/− ) mice underwent partial carotid ligation induce left carotid. In addition,...
Abstract Endothelial cells (ECs) are a highly specialized and heterogeneous population that plays fundamental role in maintaining vascular homeostasis, immune regulation, blood flow control. Beyond serving as physical barrier, ECs exhibit remarkable plasticity, undergoing phenotypic transitions, including endothelial-to-mesenchymal (EndMT), endothelial-to-hematopoietic (EndHT), endothelial-to-osteoblast (EndOT) endothelial-to-immune-cell-like (EndICLT). These transitions allow to adapt...
Hypertension is a complex condition and common cardiovascular risk factor. Dietary docosahexaenoic acid (DHA) modulates atherosclerosis hypertension, possibly via an inflammatory mechanism. IL-1 (interleukin 1) has established role in inflammation, although whether inhibition blood pressure unclear.
Introduction Atherosclerosis is a progressive disease that develops in areas of disturbed flow (d-flow). Progressive atherosclerosis characterized by bulky plaques rich mesenchymal cells and high-grade inflammation can rupture leading to sudden cardiac death or acute myocardial infarction. In response d-flow, endothelial acquire phenotype through endothelial-to-mesenchymal transition (EndMT). However, the signaling intermediaries link d-flow EndMT are incompletely understood. Methods Results...
Although the Canakinumab Anti-Inflammatory Thrombosis Outcomes Study (CANTOS) established role of treating inflammation in atherosclerosis, our understanding endothelial activation at atherosclerosis-prone sites remains limited. Disturbed flow atheroprone regions primes plaque by enhancing NF-κB signaling. Herein, we demonstrate a for Nck adaptor proteins disturbed flow-induced activation. highly similar, only Nck1 deletion, but not Nck2 limited and proinflammatory gene expression....
Endothelial nitric oxide (NO) is a critical mediator of vascular function and remodeling. NO produced by endothelial synthase (eNOS), which activated calcium (Ca2+)-dependent Ca2+-independent pathways. Here, we report that neurogranin (Ng), regulates Ca2+-calmodulin (CaM) signaling in the brain, uniquely expressed cells (EC) human mouse vasculature, also required for eNOS regulation. To test role Ng activation, knockdown aortic (HAEC) was performed using SiRNA along with knockout (Ng −/−)...
Expression of the interleukin-1 receptor type I (IL-1RI) co-receptor Toll-like and regulator (TILRR) is significantly increased in blood monocytes following myocardial infarction atherosclerotic plaque, whereas levels healthy tissue are low. TILRR association with IL-1RI at these sites causes aberrant activation inflammatory genes, which underlie progression cardiovascular disease. The authors show that genetic deletion or antibody blocking function reduces development plaques. Lesions...
The multifunctional glycoprotein fibronectin influences several crucial cellular processes and contributes to multiple pathologies. While a link exists between fibronectin-associated pathologies the receptor tyrosine kinase EphA2, mechanism by which EphA2 promotes matrix remodeling remains unknown. We previously demonstrated that deletion reduces smooth muscle deposition blunts in atherosclerosis without influencing expression. now show expression is required for contractility-dependent...
Background Alteration in hemodynamic shear stress at atheroprone sites promotes endothelial paracellular pore formation and permeability. The molecular mechanism remains unknown. Methods Results We show that Nck (noncatalytic region of tyrosine kinase) deletion significantly ameliorates disturbed flow-induced permeability, selective isoform depletion suggests distinct signaling mechanisms. Only Nck1 reduces whereas Nck2 has no significant effects. Additionally, re-expression, but not Nck2,...
Idiopathic pulmonary arterial hypertension (IPAH) is increasingly diagnosed in elderly patients who also have an increased risk of co‐morbid atherosclerosis. Apolipoprotein E‐deficient (ApoE −/− ) mice develop atherosclerosis with severe PAH when fed a high‐fat diet (HFD) and levels endothelin (ET)‐1. ET‐1 receptor antagonists (ERAs) are used for the treatment but less known about whether ERAs beneficial We therefore examined HFD‐ApoE macitentan, dual ET A /ET B antagonist, would any effect...
Infarct size is a major determinant of outcomes after acute myocardial infarction (AMI). Carbon monoxide-releasing molecules (CORMs), which deliver nanomolar concentrations carbon monoxide to tissues, have been shown reduce infarct in rodents. We evaluated efficacy and safety CORM-A1 clinically relevant porcine model AMI. induced AMI Yorkshire White pigs by inflating coronary angioplasty balloon completely occlude the left anterior descending artery for 60 minutes, followed deflation mimic...
Abstract While CANTOS established the role of treating inflammation in atherosclerosis, our understanding endothelial activation at atherosclerosis-prone sites remains limited. Disturbed flow atheroprone regions primes plaque by enhancing NF-κB signaling. Herein, we demonstrate a novel for Nck adaptor proteins disturbed flow-induced activation. Although highly similar, only Nck1 deletion, but not Nck2 limits and proinflammatory gene expression. knockout mice show reduced both models high fat...
Abstract Venous thromboembolic events are significant contributors to morbidity and mortality in patients with stroke. Neutrophils among the first cells blood respond stroke known promote deep vein thrombosis (DVT). Integrin α9 is a transmembrane glycoprotein highly expressed on neutrophils stabilizes neutrophil adhesion activated endothelium via vascular cell molecule 1 (VCAM-1). Nevertheless, causative role of integrin poststroke DVT remains unknown. Here, we found higher plasma VCAM-1...
<h3>Backgrounds</h3> Current evidence from epidemiological studies, clinical trials and animal based research has shown an inverse relationship between omega-3 fatty acids (n3FA) cardiovascular events. Docosahexaenoic acid (DHA), a major n3FA in fish oil, been studied relation to inflammation but the exact molecular mechanisms involved remain unclear. Additionally, its role atherosclerosis requires further elucidation. Plant-derived dietary a-Linolenic (ALA) recently favourable impact on...
Endothelial cells (ECs) are critically involved in the pathogenesis of atherosclerosis by producing inflammatory mediators, including interleukin-1 beta (IL-1β). However, its mechanism externalisation is yet to be elucidated. This study investigates effect neutrophil elastase (NE) on ECs terms IL-1β release and explores underlying mechanism. Human coronary artery endothelial (HCAEC) were treated with a combination tumour necrosis factor-alpha alpha then incubated NE for 2 or 6 h. ELISA,...
<h3>Background</h3> Macrophages are a heterogeneous and diverse population of cells with an important role in immunity also the development diseases including atherosclerosis. exhibit spectrum phenotypes, from pro-inflammatory or M1/ ‘classically activated’ to anti-inflammatory M2/ ‘alternatively wound healing properties. These highly plastic can switch one phenotype another depending on environmental cues. Despite considerable work aiming characterise polarisation macrophages disease, there...
<h3>Introduction</h3> Dietary omega-3 fatty acids have been associated with protection from atherosclerosis. However, the underlying mechanisms are incompletely understood. Blood flow generate a frictional force on endothelial cells called wall shear stress (WSS) that alters vascular function. The aim of this study was to determine whether docosahexaenoic acid (DHA), an acid, modulates inflammation, blood velocity and WSS in experimental <h3>Methods</h3> ApoE<sup>–/–</sup> mice fed either...