A5076380311- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- interferon and immune responses
- Neonatal Respiratory Health Research
- Blood Coagulation and Thrombosis Mechanisms
- Immune cells in cancer
- Immune Response and Inflammation
- Inflammasome and immune disorders
- Sphingolipid Metabolism and Signaling
- Phagocytosis and Immune Regulation
- Stress Responses and Cortisol
- Hippo pathway signaling and YAP/TAZ
- Cell Adhesion Molecules Research
- Adenosine and Purinergic Signaling
- COVID-19 Clinical Research Studies
- Atherosclerosis and Cardiovascular Diseases
- Pain Mechanisms and Treatments
- Inflammation biomarkers and pathways
- Respiratory Support and Mechanisms
- Nuclear Structure and Function
- Cellular Mechanics and Interactions
- Ion Channels and Receptors
- Biochemical effects in animals
- Phosphodiesterase function and regulation
- Neurological Complications and Syndromes
- Drug Solubulity and Delivery Systems
University of Illinois Chicago
2017-2025
University of Illinois Urbana-Champaign
2019-2025
Illinois College
2019-2025
Lake Erie College of Osteopathic Medicine
2025
Center for Vascular Biology Research
2023-2024
University of Delhi
2014-2021
Shaqra University
2021
Alveolar macrophages (AMs), upon sensing pathogens, trigger host defense by activating toll-like receptor 4 (TLR4), but the counterbalancing mechanisms that deactivate AM inflammatory signaling and prevent lethal edema, hallmark of acute lung injury (ALI), remain unknown. Here, we demonstrate essential role protease-activating 2 (PAR2) in rapidly suppressing inflammation to long-lasting injury. We show thrombin, released during TLR4-induced injury, directly activates PAR2 generate cAMP,...
Acute lung injury (ALI) is a lethal inflammatory disorder whose incidence on the rise. Alveolar macrophages normally act to resolve inflammation, but when dysregulated they can provoke ALI. We demonstrate that monocyte-derived (CD11b+ macrophages) recruited into airspace upregulate anti-inflammatory function of alveolar by suppressing their stimulator type 1 interferon gene (STING) signaling. Depletion CD11b+ in mice (macrophagedep mice) after endotoxin or Pseudomonas aeruginosa causes...
Extracellular vesicles (EVs) are cell-secreted particles with broad potential to treat tissue injuries by delivering cargo program target cells. However, improving the yield of functional EVs on a per cell basis remains challenging due an incomplete understanding how microenvironmental cues regulate EV secretion at nanoscale. We show that mesenchymal stromal cells (MSCs) seeded engineered hydrogels mimic elasticity soft tissues lower integrin ligand density secrete ∼10-fold more than MSCs...
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Regenerating vascular endothelium under sepsis, trauma, and viral infections is vital for promoting the resolution of inflammatory diseases such as acute lung injury (ALI). Transient receptor potential canonical (TRPC) channels mediated Ca2+ entry compromises organ functions survival from injury. Through decoding domain in TRPC6 responsible injury, we unveiled intricate molecular mechanisms underlying regeneration injured tissue. We found that substitution isoleucine111 within Ist ankyrin...
Abstract Vascular endothelial cadherin (VE-cadherin) expressed at adherens junctions (AJs) is vital for vascular integrity and homeostasis. Here we identify the requirement of ubiquitin E3-ligase CHFR as a key mechanism ubiquitylation-dependent degradation VE-cadherin. was essential disrupting endothelium through control VE-cadherin protein expression AJs. We observe augmented in cell (EC)-restricted Chfr knockout ( ΔEC ) mice. also abrogation LPS-induced mice, suggesting pathophysiological...
Endothelial CLICs (chloride intracellular channel proteins) CLIC1 and CLIC4 are required for the GPCRs (G-protein-coupled receptors) S1PR1 (sphingosine-1-phosphate receptor 1) S1PR3 to activate small GTPases Rac1 (Ras-related C3 botulinum toxin substrate RhoA (Ras homolog family member A). To determine whether function in additional endothelial GPCR pathways, we evaluated CLIC thrombin signaling via thrombin-regulated PAR1 (protease-activated downstream effector RhoA.
The mechanical environment generated through the adhesive interaction of endothelial cells (ECs) with matrix controls nuclear tension, preventing aberrant gene synthesis and transition from restrictive to leaky endothelium, a hallmark acute lung injury (ALI). However, mechanisms controlling tension transmission nucleus EC-restrictive fate remain elusive. Here, we demonstrate that, in kinase-independent manner, focal adhesion kinase (FAK) safeguards maintain fate. In FAK-depleted ECs, robust...
Efficient phagocytosis of pathogens by the innate immune system during infectious injury is vital for restoring tissue integrity. Impaired phagocytosis, such as in case infection with Pseudomonas aeruginosa , a broad-spectrum antibiotic-resistant Gram-negative bacterium, can lead to life threatening lung disorder, acute (ALI). Evidence indicates that loss protease-activated receptor 2 (PAR2) impaired clearance leading non-resolvable ALI, but mechanism remains unclear. Here, we focused on...
Abstract Background Convalescent plasma therapy (CPT) and remdesivir (REM) have been approved for investigational use to treat coronavirus disease 2019 (COVID-19) in Nepal. Methods In this prospective, multicentered study, we evaluated the safety outcomes of treatment with CPT and/or REM 1315 hospitalized COVID-19 patients over 18 years 31 hospitals across was administered moderate, severe, or life-threatening infection. severe infections who were at high risk progression clinical worsening...
Increased lung vascular permeability and neutrophilic inflammation are hallmarks of acute injury. Alveolar macrophages (AMϕ), the predominant sentinel cell type in airspace, die massive numbers while fending off pathogens. Recent studies indicate that AMϕ pool is replenished by airspace-recruited monocytes, but mechanisms instructing conversion recruited monocytes into reparative remain elusive. Cyclic AMP (cAMP) a barrier protective immunosuppressive second messenger lung. Here, we...
Cell viability assay showing absence of toxicity in cells treated with calcium phosphate nanoparticles, without (CP) and (CP-CH) chitosan coating.
Increased endothelial permeability leads to excessive exudation of plasma proteins and leukocytes in the interstitium, which characterizes several vascular diseases including acute lung injury. The myosin light chain kinase long (MYLK-L) isoform is canonically known regulate by phosphorylating (MLC-P). Compared short MYLK isoform, MYLK-L contains an additional stretch ~919 amino acid at N-terminus unknown function. We show that thapsigargin thrombin-induced SOCE was markedly reduced...
Summary IFNγ, a type II interferon secreted by immune cells, augments tissue responses to injury following pathogenic infections leading lethal acute lung (ALI). Alveolar macrophages (AM) abundantly express Toll-like receptor-4 and represent the primary cell of innate system in lungs. A fundamental question remains whether AM generation IFNg leads uncontrolled response perpetuated injury. LPS induced sustained increase levels unresolvable inflammatory mice lacking RGS2 but not null chimeric...
: Background: Asthma is a chronic inflammatory airway disease and oxidative stress may be involved in its pathogenesis. The present study aims at evaluating the therapeutic effects of antioxidant drug Ascorbic Acid (Vitamin C) patients Bronchial Asthma. Method: Patients asthma from outpatient facility our institute were enrolled for divided into control group. Both groups given inhaled fluticasone salmeterol oral theophylline. acid was Each patient followed up weekly assessment efficacy...
Nanoparticles have special properties, such as higher surface-to-volume ratio and reactivity, which increases cell penetrability enhance their applicability in the field of medicine, especially case where other drugs are ineffective. Calcium phosphate nanoparticles (CPNP) encapsulation with therapeutic and/or diagnostic agents is an agent synthesized. However, there concerns related to colloidal stability these nanoparticles, reflected tendency form aggregates physiological milieu....
Acute respiratory distress syndrome (ARDS) is the major cause of mortality among hospitalized acute lung injury (ALI) patients. Lung macrophages play an important role in maintaining tissue-fluid homeostasis following injury.