A5083464740- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Pulmonary Hypertension Research and Treatments
- Neonatal Respiratory Health Research
- Peptidase Inhibition and Analysis
- Retinoids in leukemia and cellular processes
- Cytomegalovirus and herpesvirus research
- Adenosine and Purinergic Signaling
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Paraoxonase enzyme and polymorphisms
- Transplantation: Methods and Outcomes
- Immune Cell Function and Interaction
- Medical Imaging and Pathology Studies
- High Altitude and Hypoxia
- Heme Oxygenase-1 and Carbon Monoxide
- Sarcoidosis and Beryllium Toxicity Research
- Circadian rhythm and melatonin
- Cancer-related gene regulation
- Occupational and environmental lung diseases
- Mechanical Circulatory Support Devices
- Neonatal Health and Biochemistry
- Immunodeficiency and Autoimmune Disorders
- Neuroscience of respiration and sleep
- Pleural and Pulmonary Diseases
- Histone Deacetylase Inhibitors Research
The University of Texas Health Science Center at Houston
2014-2019
Central South University
2016
University of Colorado Denver
2016
University of Oregon
2016
Xiangya Hospital Central South University
2016
Tulane University
2013-2016
University of Turku
2016
Abstract Idiopathic pulmonary fibrosis (IPF) is a lethal lung disease with progressive and death within 2–3 y of diagnosis. IPF incidence prevalence rates are increasing annually few effective treatments available. Inhibition IL-6 results in the attenuation mice. It unclear whether this due to blockade classical signaling, mediated by membrane-bound IL-6Rα, or trans soluble IL-6Rα (sIL-6Rα). Our study assessed role sIL-6Rα IPF. We demonstrated elevations patients mice during onset...
Regulatory T (T reg) cell deficiency causes lethal, CD4+ cell–driven autoimmune diseases. Stem transplantation is used to treat these diseases, but this procedure limited by the availability of a suitable donor. The intestinal microbiota drives host immune homeostasis regulating differentiation and expansion reg, Th1, Th2 cells. It currently unclear if reg deficiency–mediated disorders can be treated targeting enteric microbiota. Here, we demonstrate that Foxp3+ results in gut microbial...
Summary Aging constitutes a significant risk factor for fibrosis, and idiopathic pulmonary fibrosis ( IPF ) is characteristically associated with advancing age. We propose that age‐dependent defects in the quality of protein cellular organelle catabolism may be causally related to fibrosis. Our research found autophagy diminished corresponding elevated levels oxidized proteins lipofuscin response lung injury old mice middle‐aged compared younger animals. More importantly, older expose are...
Background: High altitude is a challenging condition caused by insufficient oxygen supply. Inability to adjust hypoxia may lead pulmonary edema, stroke, cardiovascular dysfunction, and even death. Thus, understanding the molecular basis of adaptation high reveal novel therapeutics counteract detrimental consequences hypoxia. Methods: Using high-throughput, unbiased metabolomic profiling, we report that metabolic pathway responsible for production erythrocyte 2,3-bisphosphoglycerate...
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and fatal disease. Histone deacetylase 6 (HDAC6) alters function fate of various proteins via deacetylation lysine residues, implicated in TGF-β1-induced EMT (epithelial-mesenchymal transition). However, the role HDAC6 unknown.HDAC6 expression IPF control lungs was assessed by quantitative real-time PCR (qRT-PCR) immunoblots. Lung fibroblasts were treated with TGF-β1 ± inhibitors (Tubacin, Tubastatin, ACY1215, or MC1568), fibrotic...
BMAL1 is a transcriptional activator of the molecular clock feedback network. Besides its role in generating circadian rhythms, it has also been shown to be involved modulation cell proliferation, autophagy and cancer invasion. However, pulmonary fibrogenesis still largely unknown. In this study, we investigated crosstalk between signaling transduction cellular activities TGF-β1, key player lung fibrogenesis.Lungs from wild type TGF-β1-adenovirus-infected mice were harvested homogenized for...
Idiopathic pulmonary fibrosis (IPF) is a lethal lung disease of unknown etiology. The development hypertension (PH) considered the single most significant predictor mortality in patients with chronic diseases. processes that govern progression and fibroproliferative vascular lesions IPF are not fully understood. Using human explant samples from or without diagnosis PH as well normal control tissue, we report reduced BMPR2 expression IPF+PH. These changes were consistent dampened P-SMAD 1/5/8...
Idiopathic pulmonary fibrosis (IPF) is a deadly chronic lung disease. Extracellular accumulation of adenosine and subsequent activation the ADORA2B receptor play important roles in regulating inflammation IPF. Additionally, alternatively activated macrophages (AAMs) expressing have been implicated mediating adenosine's effects Although hypoxic conditions are present IPF, hypoxia's role as direct modulator macrophage phenotype identification factors that regulate expression on AAMs IPF not...
Idiopathic pulmonary fibrosis (IPF) is a chronic and deadly disease with poor prognosis few treatment options. Pathological remodeling of the extracellular matrix (ECM) by myofibroblasts key factor that drives pathogenesis, although underlying mechanisms remain unknown. Alternative polyadenylation (APA) has recently been shown to play major role in cellular responses stress driving expression fibrotic factors ECMs through altering microRNA sensitivity, but connection IPF not established....
Idiopathic pulmonary fibrosis (IPF) is a lethal, fibroproliferative disease. Pulmonary hypertension (PH) can develop secondary to IPF and increase mortality. Alternatively, activated macrophages (AAMs) contribute the pathogenesis of both PH. Here we hypothesized that adenosine signaling through ADORA2B on AAMs impacts progression these disorders conditional deletion myeloid cells would have beneficial effect in model diseases. Conditional knockout mice lacking (Adora2Bf/f-LysMCre) were...
Idiopathic pulmonary fibrosis (IPF) is a progressive disease of insidious onset, and responsible for up to 30,000 deaths per year in the U.S. Excessive production extracellular matrix by myofibroblasts has been shown be an important pathological feature IPF. TGF-β1 expressed fibrotic lung promotes fibroblast myofibroblast differentiation (FMD) as well deposition. To identify mechanism Arsenic trioxide’s (ATO)’s anti-fibrotic effect vitro, normal human fibroblasts (NHLFs) were treated with...
Group III pulmonary hypertension (PH) is a highly lethal and widespread lung disorder that common complication in idiopathic fibrosis (IPF) where it considered to be the single most significant predictor of mortality. While increased levels hyaluronan have been observed IPF patients, hyaluronan-mediated vascular remodelling mechanisms promoting PH associated with are not fully understood.Explanted tissue from patients without diagnosis was used identify hyaluronan. In addition, an...
Idiopathic pulmonary fibrosis (IPF) is a deadly lung disease with few therapeutic options. Apoptosis of alveolar epithelial cells, followed by abnormal tissue repair characterized hyperplastic cell formation, pathogenic process that contributes to the progression fibrosis. However, signaling pathways responsible for increased proliferation cells remain poorly understood.To investigate role deoxycytidine kinase (DCK), an important enzyme salvage deoxynucleotides, in fibrosis.DCK expression...
Group III pulmonary hypertension (PH) is a highly prevalent and deadly lung disorder with limited treatment options other than transplantation. PH affects patients ongoing chronic injury, such as idiopathic fibrosis (IPF). Between 30 40% of IPF are diagnosed PH. The diagnosis has devastating consequences to these patients, leading increased morbidity mortality, yet the molecular mechanisms involved in development disease remain elusive. Our hypothesis was that hypoxic-adenosinergic system...
Idiopathic pulmonary fibrosis is a devastating lung disease with limited treatment options. The signaling molecule adenosine produced in response to injury and serves protective role early stages of detrimental during chronic such as seen conditions fibrosis. Understanding the association extracellular levels progression critical for designing based approaches treat goal this study was use various models experimental understand when are elevated whether these elevations were associated...
Hyperoxic lung injury is characterized by cellular damage from high oxygen concentrations that lead to an inflammatory response in the with infiltration and pulmonary edema. Adenosine a signaling molecule generated extracellularly CD73 injury. Extracellular adenosine signals through cell surface receptors has been found be elevated plays protective role acute situations. In particular, ADORA2B activation However, little known about of hyperoxic We hypothesized hyperoxia-induced leads...
Myofibroblasts are important mediators of fibrogenesis; thus blocking fibroblast-to-myofibroblast differentiation (FMD) may be an effective strategy to treat pulmonary fibrosis (PF). Previously, we reported that histone deacetylase 4 (HDAC4) activity is necessary for transforming growth factor-β
Abstract We have previously shown that disruption of promyelocytic leukemia nuclear bodies (PML NBs) is sufficient to activate the EBV lytic cycle thus making infected cells susceptible ganciclovir (GCV) mediated killing in vitro . Here we show co-administration GCV and arsenic trioxide (ATO), a PML NB disruptor, reduces tumor volume xenograft model nasopharyngeal carcinoma utilizing CNE1 cells. When administered at pharmacologic levels, both ATO reduced growth while co-treatment with +...
Abstract Regulatory T-cell (Treg) deficiency causes lethal, CD4+T cell-driven autoimmune diseases. Stem cell transplantation is used to treat these diseases, but this procedure limited by the availability of a suitable donor. The intestinal microbiota drives host immune homeostasis regulating development Treg, Th1 and Th2 cells. It currently unclear if Treg-deficiency disorders can be treated targeting enteric microbiota. Our aims are determine autoimmunity, gut microbiota, plasma...