A5101688429- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Pulmonary Hypertension Research and Treatments
- MicroRNA in disease regulation
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Medical Imaging and Pathology Studies
- Cancer-related molecular mechanisms research
- Tracheal and airway disorders
- Systemic Sclerosis and Related Diseases
- IL-33, ST2, and ILC Pathways
- Neonatal Respiratory Health Research
- Occupational and environmental lung diseases
- Tissue Engineering and Regenerative Medicine
- Circular RNAs in diseases
- Estrogen and related hormone effects
- Biomarkers in Disease Mechanisms
- Autophagy in Disease and Therapy
- Lung Cancer Treatments and Mutations
- Cytomegalovirus and herpesvirus research
- Mesenchymal stem cell research
- Asthma and respiratory diseases
- Vascular Anomalies and Treatments
- Extracellular vesicles in disease
- Chemical Reactions and Isotopes
- Eosinophilic Disorders and Syndromes
- Trace Elements in Health
The Ohio State University
2021-2025
Lung Institute
2024
Schneider Electric (Germany)
2024
Technical University of Denmark
2023
University of Pittsburgh
2011-2021
University of Pittsburgh Medical Center
2018-2019
McGowan Institute for Regenerative Medicine
2014-2018
Interstitial Cystitis Association
2017
Reproductive Medicine Institute
2015
Universidad de Antioquia
2015
The mechanisms of aging that are involved in the development idiopathic pulmonary fibrosis (IPF) still unclear. Although it has been hypothesized proliferation and activation human lung fibroblasts (hLFs) essential IPF, no studies have assessed how this process works an lung. Our goal was to elucidate if there were age-related changes on primary hLFs isolated from IPF lungs compared with age-matched controls. We investigated several hallmarks patients increased cellular senescence higher...
The etiology of idiopathic pulmonary fibrosis (IPF) is unknown. Because viral pathogenesis IPF has been suggested, we have established a murine model progressive by infecting IFN-gammaR-deficient mice (IFN-gammaR(-/-)) with the gamma-herpesvirus 68. alveolar macrophages in humans implicated driving profibrotic response, studied their role our model. Chronic herpesvirus infection lung was associated recruitment to areas epithelial hyperplasia and infected lungs. Using immunohistochemistry,...
Abstract Pulmonary inflammation, which is characterized by the presence of perivascular macrophages, has been proposed as a key pathogenic driver pulmonary hypertension (PH), vascular disease with increasing global significance. However, mechanisms expansion lung macrophages and role blood-borne monocytes in PH are poorly understood. Using multicolor flow cytometric analysis blood mouse rat models patients PH, an increase was observed. In parallel, tissue displayed increased chemokine...
Rationale: Several common and rare genetic variants have been associated with idiopathic pulmonary fibrosis, a progressive fibrotic condition that is localized to the lung.Objectives: To develop an integrated understanding of located in multiple loci reported contribute risk disease.Methods: We performed deep targeted resequencing (3.69 Mb DNA) cases (n = 3,624) control subjects 4,442) across genes regions previously disease. tested for associations between disease 1) individual via logistic...
Idiopathic pulmonary fibrosis (IPF) and systemic sclerosis-associated interstitial lung disease (SSc-ILD) differ in the predominant demographics identified genetic risk alleles of effected patients, however both diseases frequently progress to respiratory failure death. Contrasting advanced SSc-ILD IPF provides insight role dysregulated immunity may play fibrosis. To analyze cell-type specific transcriptome commonalities differences between SSc-ILD, we compared single-cell RNA-sequencing...
Idiopathic pulmonary fibrosis (IPF) is the most common and devastating of interstitial lung diseases. Epithelial dysfunction thought to play a prominent role in disease pathology, we sought characterize secreted signals that may contribute pathology. Transcriptional profiling senescent type II alveolar epithelial cells from mice with epithelial-specific telomere identified transforming growth factor-β family member, differentiation factor 15 (Gdf15), as significantly upregulated protein....
Background A devastating late injury caused by radiation is pulmonary fibrosis. This risk may limit the volume of irradiation and compromise potentially curative therapy. Therefore, development a therapy to prevent this toxicity can be great benefit for patient population. Activation chemokine receptor CXCR4 its ligand stromal cell-derived factor 1 (SDF-1/CXCL12) important in radiation-induced Here, we tested whether MSX-122, novel small molecule partial antagonist, block fibrotic process....
Idiopathic pulmonary fibrosis (IPF) is a progressive, fibrotic lung disease of unknown etiology. A viral pathogenesis in IPF has been suggested since >95% patients have evidence chronic infection with one or more herpesviruses. To determine whether herpesvirus can cause fibrosis, we infected mice the murine gamma-herpesvirus 68 (MHV68). Because T helper type 2 (Th2) phenotype, used IFN-gammaR-/-, strain biased to develop Th2 responses. Chronic MHV68 IFN-gammaR-/- resulted progressive...
Background Vascular hyperproliferative disorders are characterized by excessive smooth muscle cell (SMC) proliferation leading to vessel remodeling and occlusion. In pulmonary arterial hypertension (PAH), SMC phenotype switching from a terminally differentiated contractile synthetic state is gaining traction as our understanding of the disease progression improves. While maintenance reportedly orchestrated MEF2C-myocardin (MYOCD) interplay, little known regarding molecular control at this...
Pulmonary arterial hypertension (PAH) is a rapidly degenerating and devastating disease of increased pulmonary vessel resistance leading to right heart failure. Palliative modalities remain limited despite recent endeavors investigate the mechanisms underlying vascular (PVR), i.e. aberrant remodeling occlusion. However, little known molecular responsible for endothelial proliferation, root cause PAH-associated remodeling. Lung tissue specimens from PAH non-PAH patients hypoxia-exposed human...
This study demonstrates a previously unidentified role for Notch2 in the maintenance of lung vascular endothelial cell quiescence and pulmonary artery hypertension (PAH). A key novel finding is that suppression activates Notch1 via Rb-E2F1-mediated signaling induces proliferation apoptosis resistance human cells. Notably, PAH patients show reduced levels their arteries, supporting as fundamental driver pathogenesis.
A coordinated voltage control algorithm is developed to facilitate the integration of electric vehicles into microgrids. This proposed reduces fluctuations via optimal adjustment tap positions on-load changers and reactive power injections inverter-based distributed energy resources. Based on algorithm, an industrial implementation framework established enable interactive communications among changers, resources, etc. Compared previous studies regulation in microgrids, this work...
The low resolution of spatial transcriptomics data necessitates additional information for optimal use. We developed scDOT, which combines and single cell RNA sequencing to improve the ability reconstruct resolved maps identify senescent cells. scDOT integrates transport expression deconvolution learn non-linear couplings between cells spots infer placements. Application lung improves on prior methods allows identification organization cells, their neighboring novel genes involved in...
Pulmonary hypertension (PH), a heterogeneous vascular disease, consists of subtypes with overlapping clinical phenotypes. MicroRNAs, small non‐coding RNAs that negatively regulate gene expression, have emerged as regulators PH pathogenesis. The muscle‐specific micro RNA (miR)‐204 is known to be depleted in diseased pulmonary artery smooth muscle cells (PASMCs), furthering proliferation and promoting PH. Alterations circulating plasma miR‐204 across the trans‐pulmonary bed might provide...
Reversible lysine acetylation regulates the activity of cardiac metabolic enzymes, including those controlling fuel substrate metabolism. Mitochondrial-targeted GCN5L1 and SIRT3 have been shown to regulate status mitochondrial but role that plays in driving differences between male female hearts is not currently known. In this study, we describe a significant difference levels mouse hearts, women post- premenopausal age. We further find estrogen drives expression cell line uses...
IL-25 and IL-4 signaling in the setting of infection or allergic responses can drive Type 2 inflammation. requires IL-17 receptor B (IL-17Rb) to mediate through nuclear factor κ (NF-κB) transcriptional activation. Despite known coexistence these two cytokines inflammatory environment, collaborative between axes is poorly explored. Here we demonstrate induction both IL-17Rb protein human lung tissue culture, primary alveolar macrophages, THP-1 monocytic cell line. treatment triggers gene...
Hypoxia can be damaging either because cells are directly sensitive to low oxygen pressure in their local microenvironment and/or they exposed circulating factors systemically secreted response hypoxia. The conventional hypoxia model, breathing hypoxic air, does not allow one distinguish between these and systemic effects. Here we propose validate a model for differentially applying challenges an animal. We used parabiosis, two mice sharing circulation by surgical union through the skin,...