A5088113721- Pulmonary Hypertension Research and Treatments
- Protease and Inhibitor Mechanisms
- Circular RNAs in diseases
- Cancer-related molecular mechanisms research
- ATP Synthase and ATPases Research
- Aortic aneurysm repair treatments
- Cell Adhesion Molecules Research
- Cardiovascular Function and Risk Factors
- COVID-19 Clinical Research Studies
- Respiratory Support and Mechanisms
- Adipose Tissue and Metabolism
- Mitochondrial Function and Pathology
- PI3K/AKT/mTOR signaling in cancer
- Angiogenesis and VEGF in Cancer
- Blood Coagulation and Thrombosis Mechanisms
- Coronary Interventions and Diagnostics
- Neonatal Respiratory Health Research
- Long-Term Effects of COVID-19
- MicroRNA in disease regulation
- Endoplasmic Reticulum Stress and Disease
The Ohio State University
2022-2024
Lung Institute
2023-2024
The Ohio State University Wexner Medical Center
2022
Pulmonary arterial hypertension (PAH) features pathogenic and abnormal endothelial cells (ECs), one potential origin is clonal selection. We studied the role of p53 toll-like receptor 3 (TLR3) in expansion pulmonary (PH) via regulation bone morphogenetic protein (BMPR2) signaling. ECs PAH patients had reduced expression. EC-specific knockout exaggerated PH, TLR3 expression rat lung CD117+ ECs. Reduced degradation (Nutlin 3a) abolished EC expansion, induced BMPR2, ameliorated PH....
Pulmonary arterial hypertension (PAH) is a devastating and progressive disease with limited treatment options. Endothelial dysfunction plays central role in the development progression of PAH, yet underlying mechanisms are incompletely understood. The endosome-lysosome system important to maintain cellular health, small GTPase RAB7 regulates many functions this system. Here, we explored endothelial cell (EC) function lung vascular homeostasis. We found reduced expression ECs from patients...
Pulmonary arterial hypertension (PAH) is a progressive disease characterized by vasoconstriction and remodeling of small pulmonary arteries (PAs). Central to the process switch vascular cells proliferative, apoptosis-resistant phenotype. Plasminogen activator inhibitors-1 -2 (PAI-1 PAI-2) are primary physiological inhibitors urokinase-type tissue-type plasminogen activators (uPA tPA), but their roles in PAH unsettled. Here, we report that:
ABSTRACT Cardiovascular sequelae of severe acute respiratory syndrome (SARS) coronavirus-2 (CoV-2) disease 2019 (COVID-19) contribute to the complications disease. One potential complication is lung vascular remodeling, but exact cause still unknown. We hypothesized that endothelial TLR3 insufficiency contributes remodeling induced by SARS-CoV-2. In lungs COVID-19 patients and SARS-CoV-2 infected Syrian hamsters, we discovered thickening pulmonary artery media microvascular rarefaction,...
Abstract Pulmonary arterial hypertension (PAH) is a progressive, devastating disease, and its main histological manifestation an occlusive pulmonary arteriopathy. One important functional component of PAH aberrant endothelial cell (EC) function including apoptosis‐resistance, unchecked proliferation, impaired migration. The mechanisms leading to maintaining physiologic EC are not fully understood. Here, we tested the hypothesis that in PAH, ECs have increased expression transmembrane protein...
ABSTRACT Pulmonary arterial hypertension (PAH) is a devastating and progressive disease with limited treatment options. Endothelial dysfunction plays central role in development progression of PAH, yet the underlying mechanisms are incompletely understood. The endosome-lysosome system important to maintain cellular health small GTPase RAB7 regulates many functions this system. Here, we explored endothelial cell (EC) function lung vascular homeostasis. We found reduced expression ECs from PAH...
Pulmonary arterial hypertension (PAH) is a progressive and potentially rapidly fatal disease characterized by vasoconstriction remodeling of small pulmonary arteries (PA) leading to increased vascular resistance right heart failure. Central the process switch smooth muscle cells in PAs (PASMC) proliferative, apoptosis-resistant phenotype. There reason suspect that plasminogen activator system may play an important role program PAH based on its roles post-injury restenosis, fibrosis,...
Introduction: Pulmonary arterial hypertension (PAH) is a progressive and lethal disease. The current treatment options do not target pulmonary artery endothelial cell (PAEC) dysfunction. We have previously shown role for the endosomal double stranded (ds) RNA receptor toll-like 3 (TLR3) its regulation via interleukin-10 (IL-10) in promoting PAEC dysfunction experimental (PH). Yet of cytosolic dsRNA melanoma differentiation factor 5 (MDA-5) known. Hypothesis: hypothesized that deficient...