A5038172993- Adenosine and Purinergic Signaling
- Heme Oxygenase-1 and Carbon Monoxide
- Neonatal Respiratory Health Research
- Respiratory Support and Mechanisms
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Nitric Oxide and Endothelin Effects
- Autophagy in Disease and Therapy
- TGF-β signaling in diseases
- Cardiac Fibrosis and Remodeling
- Pulmonary Hypertension Research and Treatments
- Cancer-related gene regulation
- Receptor Mechanisms and Signaling
- Endoplasmic Reticulum Stress and Disease
- Inflammasome and immune disorders
- Eicosanoids and Hypertension Pharmacology
- Phagocytosis and Immune Regulation
- Advanced Glycation End Products research
- Pneumocystis jirovecii pneumonia detection and treatment
- Effects of Radiation Exposure
- Cardiac Ischemia and Reperfusion
- MicroRNA in disease regulation
- Glutathione Transferases and Polymorphisms
- Renin-Angiotensin System Studies
- Adipose Tissue and Metabolism
- Protease and Inhibitor Mechanisms
Brown University
2013-2023
Providence VA Medical Center
2008-2022
University of Florida
2022
University of Cincinnati
2022
Providence College
2022
Rhode Island Hospital
2022
Ocean Institute
2022
Shandong First Medical University
2021
Shandong Tumor Hospital
2021
Huazhong University of Science and Technology
2018-2020
A crucial cause of the decreased bioactivity nitric oxide (NO) in cardiovascular diseases is uncoupling endothelial NO synthase (eNOS) caused by oxidative stress-mediated deficiency NOS cofactor tetrahydrobiopterin (BH(4)). The reversal eNOS might represent a novel therapeutic approach. treatment apolipoprotein E knockout (ApoE-KO) mice with resveratrol resulted up-regulation superoxide dismutase (SOD) isoforms (SOD1-SOD3), glutathione peroxidase 1 (GPx1), and catalase down-regulation NADPH...
Epidemiologic evidence indicates that cigarette smoke (CS) is associated with the development of acute lung injury (ALI). We have previously shown brief CS exposure exacerbates lipopolysaccharide (LPS)-induced ALI in vivo and endothelial barrier dysfunction vitro. In this study, we found also exacerbated Pseudomonas-induced mice. demonstrated microvascular cells (ECs) isolated from mice exposed to had a greater permeability or incomplete recovery after challenges by LPS thrombin. Histone...
Cigarette smoke (CS) is a major cause of chronic lung and cardiovascular diseases. Recent studies indicate that tobacco use also risk factor for acute injury (ALI) associated with blunt trauma. Increased endothelial cell (EC) permeability hallmark ALI. CS increases EC in vitro vivo; however, the underlying mechanism not well understood. In this study, we found only 6 h exposure to impaired barrier function vivo, an effect increased oxidative stress lungs attenuated by antioxidant...
Cigarette smoke (CS) exposure increases the risk for acute respiratory distress syndrome in humans and promotes alveolar-capillary barrier permeability lung injury animal models. However, underlying mechanisms are not well understood. Mitochondrial fusion fission essential mitochondrial homeostasis health disease. In this study, we hypothesized that CS caused endothelial via an imbalance of resultant oxidative stress dysfunction. We noted altered morphology by shortening networks causing...
The siRNA silencing approach has long been used as a method to regulate the expression of specific target genes in vitro and vivo. However, effectiveness delivery nonspecific immune-stimulatory function are limiting factors for therapeutic applications siRNAs. To overcome these limitations, we developed self-assembled micelle inhibitory RNA (SAMiRNA) nanoparticles made individually biconjugated siRNAs with hydrophilic polymer lipid on their ends characterized stability, function, vivo...
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Chitinase 3 like 1 (CHI3L1) is the prototypic chitinase-like protein mediating inflammation, cell proliferation, and tissue remodeling. Limited data suggest CHI3L1 elevated in human pulmonary arterial hypertension (PAH) associated with disease severity. Despite its importance as a regulator of injury/repair responses, relationship between vascular remodeling not well understood. We hypothesize that signaling pathways contribute to responses occur (PH). examined plasma levels severity PH...
Lung edema due to increased vascular permeability is a hallmark of acute lung injury and respiratory distress syndrome. Both p38 RhoA signaling events are involved in transforming growth factor (TGF)-β 1 -increased endothelial permeability; however, the mechanism by which these pathways cooperate not clear. In this study, we hypothesized that TGF-β -induced changes monolayer activation dependent on Smad2 signaling. We assessed role . found caused phosphorylation between 0.5 h exposure cells....
We have previously demonstrated that adenosine plus homocysteine enhanced endothelial basal barrier function and protected against agonist-induced dysfunction in vitro through attenuation of RhoA activation by inhibition isoprenylcysteine-O-carboxyl methyltransferase. In the current study, we tested effect elevated on pulmonary vivo. noted alone dose dependently function. While receptor A(1) or A(3) antagonists were ineffective, an transporter inhibitor, NBTI, a combination DPMX MRS1754, for...
Right ventricular (RV) dysfunction is associated with numerous smoking-related illnesses, including chronic obstructive pulmonary disease (COPD), in which it present even the absence of hypertension. It unknown whether exposure to cigarette smoke (CS) has direct effects on RV function and cardiac fibroblast (CF) proliferation or collagen synthesis. In this study, we evaluated fibrosis mice exposed CS determined mechanisms smoke-induced changes CF signaling fibrosis. AKR were for 6 wk...
Epidemiological studies indicate that cigarette smoking (CS) increases the risk and severity of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). The mechanism is not understood, at least in part because lack animal models reproduce key features CS priming process. In this study, using two strains mice, we characterized a double-hit mouse model ALI induced by caused lipopolysaccharide (LPS). C57BL/6 AKR mice were preexposed to briefly (3 h) or subacutely wk) before...
Background Cancer immunotherapy has taken center stage in cancer treatment. However, the current immunotherapies only benefit a small proportion of patients with cancer, necessitating better understanding mechanisms tumor immune evasion and improved strategies. Regulatory T (Treg) cells play an important role maintaining tolerance through inhibiting effector T-cell function. In microenvironment, Treg are used by to counteract cell-mediated suppression. Targeting may thus unleash antitumor...
The cerebral protective effects of 4-week treatment with candesartan (0.3, 1, 3 mg/kg/day) and ramipril (0.5, 1.5, 5 were examined in spontaneous hypertensive rats 24 h after middle artery occlusion. We found that both could reduce the infarct volume neurological deficit scores compared control. Importantly, neuroprotective (1 abolished by PD123319 (an AT2 receptor antagonist, 10 mg/kg/day). AT1 gene expression was downregulated while upregulated candesartan. It is concluded appears to...
Pulmonary endothelial cell (EC) apoptosis has been implicated in the pathogenesis of emphysema. Cigarette smoke (CS) causes lung EC and In this study, we show that CS exposure increased tissue adenosine levels mice, an effect associated with development Adenosine a protective against via receptor-mediated signaling. However, sustained elevated increases alveolar deaminase-deficient mice. We established vitro model by incubating presence deaminase inhibitor, deoxycoformicin. demonstrated...
Extracellular ATP, adenosine (Ado), and plus homocysteine (Ado/HC) cause apoptosis of cultured pulmonary artery endothelial cells through the enhanced formation intracellularS-adenosylhomocysteine disruption focal adhesion complexes. Because an increased intracellular ratio ofS-adenosylhomocysteine/S-adenosylmethionine favors inhibition methylation, we hypothesized that Ado/HC might act by isoprenylcysteine-O-carboxyl methyltransferase (ICMT). We found...
We have previously shown that transforming growth factor (TGF)-beta1 protected against main pulmonary artery endothelial cell (PAEC) apoptosis induced by serum deprivation and VEGF receptor blockade through a mechanism associated with ALK5-mediated Bcl-2 upregulation. In the current study, we investigated effect of TGF-beta1 on microvascular (PMVEC) apoptosis. found that, in contrast to results seen conduit PAEC, caused PMVEC, an was also dependent ALK5 activity. noted non-SMAD signaling...
Transforming growth factor (TGF)-beta1 has been reported to cause endothelial cell apoptosis. However, conflicting data have also demonstrated that TGF-beta1 promotes survival. In this study, the effect of on apoptosis cultured bovine pulmonary artery cells (PAEC) induced by multiple stimuli was investigated. protected against PAEC serum deprivation or VEGF receptor inhibitor SU-5416, but not UV light exposure TNFalpha. Neither caspase-8 nor caspase-12 activated blocker. blockade receptors...