A5090947054- Aortic aneurysm repair treatments
- Immune cells in cancer
- Macrophage Migration Inhibitory Factor
- Muscle Physiology and Disorders
- Fatty Acid Research and Health
- Phagocytosis and Immune Regulation
- Immune Response and Inflammation
- MicroRNA in disease regulation
- Transplantation: Methods and Outcomes
- RNA modifications and cancer
- Eicosanoids and Hypertension Pharmacology
- Genetic Neurodegenerative Diseases
- Signaling Pathways in Disease
- Extracellular vesicles in disease
- Cancer-related molecular mechanisms research
- Advanced Glycation End Products research
- Infectious Aortic and Vascular Conditions
- Muscle metabolism and nutrition
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- S100 Proteins and Annexins
- RNA regulation and disease
- Occupational and environmental lung diseases
- Cancer, Lipids, and Metabolism
- Cardiac Ischemia and Reperfusion
- Inflammation biomarkers and pathways
University of Florida
2020-2024
Carolinas Medical Center
2018-2023
Florida College
2021
École Normale Supérieure de Lyon
2018
Centre Hospitalier Universitaire de Lille
2017
Pannexin-1 (Panx1) channels have been shown to regulate leukocyte trafficking and tissue inflammation but the mechanism of Panx1 in chronic vascular diseases like abdominal aortic aneurysms (AAA) is unknown. Here we demonstrate that on endothelial cells, not smooth muscle orchestrate a cascade signaling events mediate remodeling. Mechanistically, cells acts as conduit for ATP release stimulates macrophage activation via P2X7 receptors mitochondrial DNA increase IL-1β HMGB1 secretion....
Abstract Abdominal aortic aneurysm (AAA) formation is characterized by inflammation, leukocyte infiltration, and vascular remodeling. Resolvin D1 (RvD1) derived from ω‐3 polyunsaturated fatty acids involved in the resolution phase of chronic inflammatory diseases. The aim this study was to decipher protective role RvD1 via formyl peptide receptor 2 (FPR2) signaling attenuating abdominal aneurysms (AAA). elastase‐treatment model AAA C57BL/6 (WT) mice human tissue used confirm our hypotheses....
The specialized pro-resolving lipid mediator maresin 1 (MaR1) is involved in the resolution phase of tissue inflammation. It was hypothesized that exogenous administration MaR1 would attenuate abdominal aortic aneurysm (AAA) growth a cytokine-dependent manner via LGR6 receptor signaling and macrophage-dependent efferocytosis smooth muscle cells (SMCs). AAAs were induced C57BL/6 wild-type (WT) mice cell specific TGF-β2 knockout (SMC-TGFβr2−/−) using topical elastase AAA model. treatment...
Patients with end stage lung diseases require transplantation (LTx) that can be impeded by ischemia-reperfusion injury (IRI) leading to subsequent chronic allograft dysfunction (CLAD) and inadequate outcomes.
Muscular dystrophy-dystroglycanopathies (MDDGs) resulting from fukutin-related protein (FKRP) gene mutations are rare disorders that result in a wide spectrum of clinical severity based on the age onset, degree myogenic atrophy, and/or neurologic involvement. There is no cure for any FKRP-related disorders, and few options available symptom management. Herein, we examine longitudinal effects dose-escalation study to evaluate safety therapeutic potential FKRP gene-replacement therapy p.P448L...
Dystroglycanopathy, a subgroup of muscular dystrophies, is characterized by hypoglycosylation α-dystroglycan (α-DG), which reduces its laminin-binding activity to extracellular matrix proteins, causing progressive loss muscle integrity and function. Mutations in the fukutin-related protein (FKRP) gene are most common causes dystroglycanopathy. FKRP transfers ribitol-5-phosphate O-mannosyl glycan on α-DG from substrate cytidine diphosphate (CDP)-ribitol, synthesized isoprenoid synthase...
Limb Girdle Muscular Dystrophy 2I (LGMDR9) is one of the most common LGMD characterized by defects in glycosylation α-dystroglycan (matriglycan) resulting from mutations Fukutin-related protein (FKRP). There no effective therapy currently available. We recently demonstrated that ribitol supplement increases levels matriglycan cells vitro and FKRP-P448L ( P448L ) mutant mouse model through drinking water administration. To be clinically relevant, we have now conducted a dose-escalating...
Muscular dystrophy-dystroglycanopathies comprise a heterogeneous and complex group of disorders caused by loss-of-function mutations in multitude genes that disrupt the glycobiology α-dystroglycan, thereby affecting its ability to function as receptor for extracellular matrix proteins. Of various involved, FKRP codes protein plays critical role maturation novel glycan found only on α-dystroglycan. Yet despite knowing genetic cause FKRP-related dystroglycanopathies, molecular pathogenesis...
ABSTRACT BACKGROUND Post-lung transplantation (LTx) injury can involve sterile inflammation due to ischemia-reperfusion (IRI). We investigated the cell-specific role of ferroptosis (excessive iron-mediated cell death) in mediating lung IRI and determined if specialized pro-resolving mediators such as Lipoxin A4 (LxA 4 ) protect against IRI. METHODS Single-cell RNA sequencing tissue from post-LTx patients was analyzed. Lung evaluated C57BL/6 (WT), formyl peptide receptor 2 knockout ( Fpr2 −/−...
Abstract Abdominal aortic aneurysm (AAA) formation is a chronic vascular pathology characterized by inflammation, leukocyte infiltration, and remodeling. The aim of this study was to delineate the protective role Resolvin D2 (RvD2), bioactive isoform specialized pro‐resolving lipid mediators, via G‐protein‐coupled receptor 18 (GPR18) signaling in attenuating AAAs. Importantly, RvD2 GPR18 levels were significantly decreased tissue AAA patients compared with controls. Furthermore, using an...
In this study, we tested the hypothesis that endogenous expression of specialized pro-resolving lipid mediators (SPMs) facilitate resolution inflammation, specifically Resolvin D1and -D2, as well Maresin1 (MaR1), can impact abdominal aortic aneurysm (AAA) formation and progression in a sex-specific manner. SPM was quantified tissue from human AAA samples murine vivo model via liquid chromatography-tandem mass spectrometry. mRNA for receptors FPR2, LGR6, GPR18 were by real-time polymerase...
ABSTRACT Abdominal aortic aneurysm (AAA) formation is a chronic vascular pathology characterized by inflammation, leukocyte infiltration and remodeling. The aim of this study was to delineate the protective role Resolvin D2 (RvD2), bioactive isoform specialized proresolving lipid mediators, via G-protein coupled receptor 18 (GPR18) signaling in attenuating AAAs. Importantly, RvD2 GPR18 levels were significantly decreased tissue AAA patients compared with controls. Furthermore, using an...
Lung transplantation (LTx) outcomes are impeded by ischemia/reperfusion injury (IRI) and subsequent chronic lung allograft dysfunction (CLAD). We examined the undefined role of receptor Mer tyrosine kinase (MerTK) on monocytic myeloid-derived suppressor cells (M-MDSCs) in efferocytosis to facilitate resolution IRI. Single-cell RNA sequencing tissue bronchoalveolar lavage (BAL) from patients after LTx were analyzed. Murine hilar ligation allogeneic orthotopic models IRI used with BALB/c (WT),...
Abstract Ischemia-reperfusion injury (IRI) after lung transplantation results in primary graft dysfunction leading to acute and chronic rejection. We investigated the role of monocytic myeloid-derived suppressor cells (M-MDSCs) mediate inflammation-resolution IRI. A murine model hilar ligation was used Balb/c (WT) cebpβ −/−(M-MDSC deficient) mice. Lung function, inflammation M-MDSC infiltration were assessed 6- or 24hrs mice undergoing sham control IRI surgeries. CD11b +Ly6G −Ly6C +iNOS...
Background: Abdominal aortic aneurysms (AAA) are characterized by thrombus formation, inflammation, and vascular remodeling. This study investigates the role of ferroptosis, an iron-dependent non-apoptotic cell death pathway, its pharmacologic inhibition in pathogenesis AAA formation. Methods: AAAs were induced 8- to 12-week old male C57BL/6 mice using topical 0.4 U/ml type 1 porcine pancreatic elastase treatment, or deactivated as control. Mice group treated with liproxstatin-1 (selective...
Abstract Ischemia-reperfusion injury (IRI) after lung transplantation entails dysregulation of inflammation-resolution pathways leading to primary graft dysfunction. We investigated the role ω-3-derived specialized pro-resolving lipid mediators, i.e. Lipoxin A4 (LxA4), and formyl peptide receptor (FPR2) signaling in resolution IRI. used an established murine model hilar ligation for IRI using C57BL/6 wild-type (WT) FPR2−/− mice that underwent sham surgery or (1hr left ischemia followed by 6-...