A5063006196- Asthma and respiratory diseases
- Autophagy in Disease and Therapy
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Cancer, Hypoxia, and Metabolism
- Metabolism and Genetic Disorders
- Extracellular vesicles in disease
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Mitochondrial Function and Pathology
- PI3K/AKT/mTOR signaling in cancer
- IL-33, ST2, and ILC Pathways
- Respiratory and Cough-Related Research
- Allergic Rhinitis and Sensitization
- Genomics, phytochemicals, and oxidative stress
- Heme Oxygenase-1 and Carbon Monoxide
- Genomics and Rare Diseases
- Eosinophilic Esophagitis
- NF-κB Signaling Pathways
- Epigenetics and DNA Methylation
- RNA modifications and cancer
- Inhalation and Respiratory Drug Delivery
- Medical Imaging and Pathology Studies
- Cytokine Signaling Pathways and Interactions
- Pulmonary Hypertension Research and Treatments
- Redox biology and oxidative stress
- Polyamine Metabolism and Applications
Nihon University
2016-2025
Juntendo University
2021
Respiratory Clinical Trials
2018
Cornell University
2013-2017
NewYork–Presbyterian Hospital
2014-2017
New York Hospital Queens
2014-2017
Presbyterian Hospital
2016-2017
Harvard University
2012-2016
Brigham and Women's Hospital
2012-2016
Beth Israel Deaconess Medical Center
2013
The pathogenesis of chronic obstructive pulmonary disease (COPD) remains unclear, but involves loss alveolar surface area (emphysema) and airway inflammation (bronchitis) as the consequence cigarette smoke (CS) exposure. Previously, we demonstrated that autophagy proteins promote lung epithelial cell death, dysfunction, emphysema in response to CS; however, underlying mechanisms have yet be elucidated. Here, using cultured cells murine models, CS causes mitochondrial dysfunction is...
Chronic obstructive pulmonary disease (COPD) involves aberrant airway inflammatory responses to cigarette smoke (CS) that are associated with epithelial cell dysfunction, cilia shortening, and mucociliary clearance disruption. Exposure CS reduced length induced autophagy in vivo differentiated mouse tracheal cells (MTECs). Autophagy-impaired (Becn1+/- or Map1lc3B-/-) mice MTECs resisted CS-induced shortening. Furthermore, increased the autophagic turnover of ciliary proteins, indicating may...
Background Epithelial cell death is a major contributor to fibrogenesis in the lung. In this study, we sought determine function of mitochondria and their clearance (mitophagy) alveolar epithelial fibrosis. Methods We studied markers mitochondrial injury mitophagy marker, PTEN-induced putative kinase 1 (PINK1), IPF lung tissues by Western blotting, transmission electron microscopy (TEM), immunofluorescence. vitro experiments were carried out cells stimulated with transforming growth...
The cytoprotective enzyme heme oxygenase-1 (HO-1) is often overexpressed in different types of cancers and promotes cancer progression. We have recently shown that the Ras-Raf-ERK pathway induces HO-1 to promote survival renal cells. Here, we examined possible mechanisms underlying HO-1-mediated cell survival. Considering growing evidence about significance apoptosis autophagy cancer, tried investigate how controls these events regulate Rapamycin (RAPA) sorafenib, two commonly used drugs for...
Autophagy plays a pivotal role in cellular homeostasis and adaptation to adverse environments, although the regulation of this process remains incompletely understood. We have recently observed that caveolin-1 (Cav-1), major constituent lipid rafts on plasma membrane, can regulate autophagy cigarette smoking-induced injury lung epithelium, underlying molecular mechanisms remain In present study we found Cav-1 interacted with regulated expression ATG12-ATG5, an ubiquitin-like conjugation...
Small-cell lung cancer (SCLC) is a highly aggressive with poor prognosis, due to lack of therapeutic targets. Sulforaphane (SFN) an isothiocyanate derived from cruciferous vegetables and has shown anticancer effects against numerous types cancer. However, its effect SCLC remains unclear. The present study aimed demonstrate the SFN in cells by investigating cell death (ferroptosis, necroptosis caspase inhibition). human lines NCI-H69, NCI-H69AR (H69AR) NCI-H82 normal bronchial epithelial...
The mechanisms by which lung structural cells survive toxic exposures to cigarette smoke (CS) are not well defined but may involve proper disposal of damaged mitochondria macro-autophagy (mitophagy), processes that be influenced pro-apoptotic ceramide (Cer) or its precursor dihydroceramide (DHC). Human epithelial and endothelial exposed CS exhibited mitochondrial damage, signaled phosphatase tensin homolog-induced putative kinase 1 (PINK1) phosphorylation, autophagy, necroptosis. Although...
Although the pathogenesis of pulmonary fibrosis remains unclear, it is known to involve epithelial injury and epithelial-mesenchymal transformation (EMT) as a consequence cigarette smoke (CS) exposure. Moreover, smoking deposits iron in mitochondria alveolar cells. Iron overload causes Fenton reaction, leading reactive oxygen species (ROS) production, ROS leakage from induces cell inflammation lungs. Nevertheless, mechanisms underlying metabolism are yet be elucidated. In this study, we...
The zinc finger protein A20 is encoded by an immediate early response gene and acts as inhibitor of nuclear factor (NF)-kappaB-dependent expression induced different stimuli, including tumor necrosis factor-alpha (TNF-alpha) interleukin-1beta (IL-1beta). Toll-like receptor 2 (TLR2) TLR4 have been found to transduce, respectively, peptidoglycan (PGN) lipopolysaccharide (LPS) signals for the activation NF-kappaB production inflammatory cytokines. Here, we examined role in TLR-mediated...
The mammalian target of rapamycin complex 1 (mTORC1) is hyperactive in many human cancers and tuberous sclerosis (TSC). Autophagy, a key mTORC1-targeted process, critical determinant metabolic homeostasis. Metabolomic profiling was performed to elucidate the cellular consequences autophagy dysregulation under conditions mTORC1. It discovered that TSC2-null cells have distinctive autophagy-dependent pentose phosphate pathway (PPP) alterations. This accompanied by enhanced glucose uptake...