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American Journal of Physiology. Lung Cellular and Molecular Physiology

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https://www.readbyqxmd.com/read/28213473/central-role-of-t-helper-17-cells-in-chronic-hypoxia-induced-pulmonary-hypertension
#1
Levi D Maston, David T Jones, Wieslawa Giermakowska, Tamara A Howard, Judy L Cannon, Wei Wang, Yongyi Wei, Weimin Xuan, Thomas C Resta, Laura V Gonzalez Bosc
RATIONALE: Inflammation is a prominent pathologic feature in pulmonary arterial hypertension as demonstrated by pulmonary vascular infiltration of inflammatory cells, including T and B lymphocytes. However, the contribution of the adaptive immune system is not well characterized in pulmonary hypertension caused by chronic hypoxia. CD4(+) T cells are required for initiating and maintaining inflammation, suggesting these cells could play an important role in the pathogenesis of hypoxic pulmonary hypertension...
February 17, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28213472/%C3%AE-2-microglobulin-participates-in-development-of-lung-emphysema-by-inducing-lung-epithelial-cells-senescence
#2
Na Gao, Ying Wang, Chun-Ming Zheng, Yan-Li Gao, Hui Li, Yan Li, Ting-Ting Fu, Li-Li Xu, Wei Wang, Sun Ying, Kewu Huang
β2-microglobulin (β2m), the light chain of major histocompatibility complex class 1 (MHC I), has been identified as a pro-aging factors and involved in the pathogenesis of neurodegenerative disorders by driving cognitive and regenerative impairments. However, little attention has focused on the effect of β2m in development of lung emphysema. Here, we found that concentrations of β2m in plasma were significantly elevated in patients with lung emphysema than those in normal control subjects (1.89 ± 0.12 mg/l vs 1...
February 17, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28213471/attenuation-of-endoplasmic-reticulum-stress-by-caffeine-ameliorates-hyperoxia-induced-lung-injury
#3
Ru-Jeng Teng, Xigang Jing, Teresa Michalkiewicz, Adeleye J Afolayan, Tzong-Jin Wu, Girija G Konduri
Rodent pups exposed to hyperoxia develop lung changes similar to bronchopulmonary dysplasia (BPD) in extremely premature infants. Oxidative stress from hyperoxia can injure developing lungs through endoplasmic reticulum (ER) stress. Early caffeine treatment decreases the rate of BPD, but the mechanisms remain unclear. We hypothesized that caffeine attenuates hyperoxia-induced lung injury through its chemical chaperone property. Sprague-Dawley rat pups were raised either in 90% (hyperoxia) or 21% (normoxia) oxygen from postnatal day 1 (P1) to postnatal day 10 (P10) and then recovered in 21% oxygen until P21...
February 17, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28213470/higher-mini-bal-total-protein-concentration-in-early-ards-predicts-faster-resolution-of-lung-injury-measured-by-more-ventilator-free-days
#4
Carolyn M Hendrickson, Jason Abbott, Hanjing Zhuo, Kathleen D Liu, Carolyn S Calfee, Michael A Matthay
The protein concentration of alveolar edema fluid in acute respiratory distress syndrome (ARDS) is dynamic. It reflects alveolar flooding during acute injury as well as fluid and protein clearance over time. We hypothesized that among ARDS patients treated with low tidal volume ventilation, higher concentrations of protein in mini-bronchoalveolar lavage (mBAL) samples would predict slower resolution of lung injury and worse clinical outcomes. Total protein and IgM concentrations in Day 0 mBAL samples from 79 subjects enrolled in the aerosolized albuterol (ALTA) ARDS Network Albuterol trial were measured by colorimetric assay and ELISA respectively...
February 17, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28213469/insulin-signaling-via-the-pi3k-akt-pathway-regulates-airway-glucose-uptake-and-barrier-function-in-a-cftr-dependent-manner
#5
Samuel A Molina, Hannah K Moriarty, Danny T Infield, Barry R Imhoff, Rachel J Vance, Agnes H Kim, Jason M Hansen, William R Hunt, Michael Koval, Nael A McCarty
Cystic fibrosis-related diabetes (CFRD) is the most common co-morbidity associated with cystic fibrosis (CF) and correlates with increased rates of lung function decline. Since glucose is a nutrient present in the airways of patients with bacterial airway infections and since insulin controls glucose metabolism, the effect of insulin on CF airway epithelia was investigated to determine the role of insulin receptors and glucose transport in regulating glucose availability in the airway. The response to insulin by human airway epithelial cells was characterized by qPCR, immunoblot, immunofluorescence, and glucose uptake assays...
February 17, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28213468/microencapsulation-of-lefty-secreting-engineered-cells-for-pulmonary-fibrosis-therapy-in-mice
#6
Hongge Ma, Shupei Qiao, Zeli Wang, Shuai Geng, Yufang Zhao, Xiaolu Hou, Weiming Tian, Xiongbiao Chen, Lifen Yao
Idiopathic pulmonary fibrosis (IPF) is a progressive disease that causes unremitting deposition of extracellular matrix proteins, thus resulting in distortion of the pulmonary architecture and impaired gas exchange. Associated with high morbidity and mortality, IPF is generally refractory to current pharmacological therapies. Lefty A, a potent inhibitor of transforming growth factor (TGF)-β signaling, has been shown to have promising antifibrotic ability in vitro for the treatment of renal fibrosis and other potential organ fibroses...
February 17, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28213467/hypoxia-induces-arginase-ii-expression-and-increases-viable-human-pulmonary-artery-smooth-muscle-cell-numbers-via-ampk%C3%AE-1-signaling
#7
Jianjing Xue, Leif D Nelin, Bernadette Chen
Pulmonary artery smooth muscle cell (PASMC) proliferation is one of the hallmark features of hypoxia-induced pulmonary hypertension. With only supportive treatment options available for this life threatening disease, treating and preventing the proliferation of PASMCs is a viable therapeutic option. A key promoter of hypoxia-induced increases in the number of viable human PASMCs is arginase II, with attenuation of viable cell numbers following pharmacologic inhibition or siRNA knockdown of the enzyme. Additionally, increased levels of arginase have been demonstrated in the pulmonary vasculature of patients with pulmonary hypertension...
February 17, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28188225/inflammation-induced-caveolin-1-and-bmprii-depletion-promotes-endothelial-dysfunction-and-tgf%C3%AE-driven-pulmonary-vascular-remodeling
#8
Suellen Darc Santos Oliveira, Maricela Castellon, Jiwang Chen, Marcelo G Bonini, Xiaowu Gu, Michael H Elliott, Roberto F Machado, Richard D Minshall
Endothelial cell (EC) activation and vascular injury are hallmark features of Acute Lung Injury and Acute Respiratory Distress Syndrome (ALI/ARDS). Caveolin-1 (Cav-1) is highly expressed in pulmonary microvascular ECs and plays a key role in maintaining vascular homeostasis. The aim of this study was to determine whether the lung inflammatory response to Escherichia coli lipopolysaccharide (LPS) promotes priming of ECs via Cav-1 depletion and whether this contributes to the onset of pulmonary vascular remodeling...
February 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28188224/lung-pericyte-like-cells-are-functional-immune-sentinel-cells
#9
Chi F Hung, Kristen L Mittelsteadt, Rena Brauer, Bonnie L McKinney, Teal S Hallstrand, William C Parks, Peter Chen, Lynn M Schnapp, W Conrad Liles, Jeremy S Duffield, William A Altemeier
Pericytes are perivascular PDGFRβ+ stromal cells required for vasculogenesis and maintenance of microvascular homeostasis in many organs. Because of their unique juxtaposition to microvascular endothelium, lung PDGFRβ+ cells are well situated to detect pro-inflammatory molecules released following epithelial injury and promote acute inflammatory responses. Thus, we hypothesized that these cells represent an unrecognized immune surveillance or injury-sentinel interstitial cell. To evaluate this hypothesis, we isolated PDGFRβ+ cells from murine lung and demonstrated that they have characteristics consistent with a pericyte population (referred to as pericyte-like cells for simplicity hereafter)...
February 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28188223/hypoxic-proliferation-requires-egfr-mediated-erk-activation-in-human-pulmonary-microvascular-endothelial-cells
#10
Hilary A White, Yi Jin, Louis G Chicoine, Bernadette Chen, Yusen Liu, Leif D Nelin
We have previously shown that hypoxic proliferation of human pulmonary microvascular endothelial cells (hPMVEC) depends on epidermal growth factor receptor (EGFR) activation. To determine down-stream signaling leading to proliferation, we tested the hypothesis that hypoxia-induced proliferation in hPMVEC would require EGFR-mediated activation of extracellular signal-regulated kinase (ERK) leading to arginase II induction. To test this hypothesis, hPMVEC were incubated in either normoxia (21% O2, 5% CO2) or hypoxia (1% O2, 5% CO2) and western blotting was performed for EGFR, arginase II, phosphorylated-ERK (pERK), and total ERK (ERK)...
February 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28130264/vagal-innervation-is-required-for-pulmonary-function-phenotype-in-htr4-mice
#11
John House, Cody E Nichols, Huiling Li, Christina Brandenberger, Rohan Virgincar, Laura Miller, Bastiaan Driehuys, Darryl C Zeldin, Stephanie London
Human genome-wide association studies (GWASs) have identified over 50 loci associated with pulmonary function and related phenotypes, yet follow-up studies to determine causal genes or variants are rare. Single nucleotide polymorphisms (SNPs) in serotonin receptor 4 (HTR4) are associated with human pulmonary function in genome-wide association studies and follow-up animal work has demonstrated that Htr4 is causally associated with pulmonary function in mice, although the precise mechanisms were not identified...
January 27, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28130263/magnetic-resonance-imaging-of-disease-progression-and-resolution-in-a-transgenic-mouse-model-of-pulmonary-fibrosis
#12
Zackary I Cleveland, Yu Michael Zhou, Teckla G Akinyi, R Scott Dunn, Cynthia R Davidson, Jinbang Guo, Jason C Woods, William D Hardie
Pulmonary fibrosis contributes to morbidity and mortality in a range of diseases, and there are no approved therapies for reversing its progression. To understand the mechanisms underlying pulmonary fibrosis and assess potential therapies, mouse models are central to basic and translational research. Unfortunately, metrics commonly used to assess murine pulmonary fibrosis require animals to be grouped and sacrificed, increasing experimental difficulty and cost. We examined the ability of three magnetic resonance imaging (MRI)-derived metrics (mean weighted lung signal, percent high signal volume, and signal coefficient of variation) to non-invasively assess lung fibrosis progression and resolution in a doxycycline (Dox) regulatable, transgenic mouse model that overexpresses transforming growth factor alpha (TGF-α) under control of a lung-epithelial-specific promoter...
January 27, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28130262/protein-biomarkers-associated-with-primary-graft-dysfunction-following-lung-transplantation
#13
Barbara Cs Hamilton, Jasleen Kukreja, Lorraine B Ware, Michael A Matthay
Severe primary graft dysfunction affects 15-20% of lung transplantation recipients and carries a high mortality risk. In addition to known donor, recipient, and perioperative clinical risk factors, numerous biologic factors are thought to contribute to primary graft dysfunction. Our current understanding of the pathogenesis of lung injury and primary graft dysfunction emphasizes multiple pathways leading to lung endothelial and epithelial injury. Biomarkers specific to these pathways can be measured in the plasma, bronchoalveolar lavage fluid, and lung tissue...
January 27, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28130261/impact-of-thrombosis-on-pulmonary-endothelial-injury-and-repair-following-sepsis
#14
Colin Evans, You-Yang Zhao
The prevailing morbidity and mortality in sepsis are largely due to multiple organ dysfunction (MOD), most commonly lung injury, as well as renal and cardiac dysfunction. Despite recent advances in defining many aspects of the pathogenesis of sepsis-related MOD, including acute respiratory distress syndrome (ARDS), there are currently no effective pharmacological or cell-based treatments for the disease. Human and animal studies have shown that pulmonary thrombosis is common in sepsis-induced ARDS, and pre-clinical studies have shown that anti-coagulation may improve outcome following sepsis challenge...
January 27, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28130260/leonardo-da-vinci-engineer-bioengineer-anatomist-and-artist
#15
John B West
Leonardo da Vinci (1452-1519) enjoys a reputation as one of the most talented people of all time in the history of science and the arts. However little attention has been given to his contributions to physiology. One of his main interests was engineering, and he was fascinated by structural problems, and the flow patterns of liquids. He also produced a large number of ingenious designs for warfare, and a variety of highly original flying machines. But of particular interest to us are his contributions to bioengineering, and how he used his knowledge of basic physical principles to throw light on physiological function...
January 27, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28130259/prenatal-exposure-to-tobacco-smoke-sex-dependently-influences-methylation-and-mrna-levels-of-the-igf-axis-in-lungs-of-mouse-offspring
#16
Karolin F Meyer, Susanne Krauss-Etschmann, Wierd Kooistra, Marjan Reinders-Luinge, Wim Timens, Lester Kobzik, Torsten Plösch, Machteld N Hylkema
BACKGROUND: Prenatal smoke exposure is a risk factor for abnormal lung development and increased sex-dependent susceptibility for asthma and COPD. Birth cohort studies show genome wide DNA methylation changes in children from smoking mothers, but evidence for sex-dependent smoke-induced effects is limited. The insulin-like growth factor (IGF) system plays an important role in lung development. We hypothesized that prenatal exposure to smoke induces lasting changes in promoter methylation patterns of Igf1 and Igf1r, thus influencing transcriptional activity, and contributing to abnormal lung development...
January 27, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28130258/hypoxia-inhibits-expression-and-function-of-mitochondrial-thioredoxin-2-to-promote-pulmonary-hypertension
#17
Sherry E Adesina, Brandy E Wade, Kaiser M Bijli, Bum-Yong Kang, Clintoria R Williams, Jing Ma, Young-Mi Go, C Michael Hart, Roy L Sutliff
Pulmonary hypertension (PH) is characterized by increased pulmonary vascular resistance, pulmonary vascular remodeling, and increased pulmonary vascular pressures that often result in right ventricular dysfunction, leading to right heart failure. Evidence suggests that reactive oxygen species (ROS) contribute to PH pathogenesis by altering pulmonary vascular cell proliferation and intracellular signaling pathways. However, the role of mitochondrial antioxidants and oxidant-derived stress signaling in the development of hypoxia-induced PH is largely unknown...
January 27, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28130257/hydrogen-peroxide-is-a-critical-regulator-of-the-hypoxia-induced-alterations-of-store-operated-ca2-entry-into-rat-pulmonary-arterial-smooth-muscle-cells
#18
Taoxiang Chen, Xiaoya Xu, Zhao Zhao, Fangyu Zhao, Yimei Gao, Xiaohong Yan, Yu Wan
To investigate the association between store-operated Ca2+ entry (SOCE) and reactive oxygen species (ROS) during hypoxia, this study determined the changes of transient receptor potential canonical 1 (TRPC1) and Orai1, two candidate proteins for store-operated Ca2+ (SOC) channels and their gate regulator, stromal interaction molecule 1 (STIM1) in a hypoxic environment and their relationship with ROS in pulmonary arterial smooth muscle cells (PASMCs). Exposing to hypoxia, a transient Ca2+ spike and subsequent Ca2+ plateau of SOCE in PASMCs were intensified when TRPC1, STIM1 and Orai1 were upregulated...
January 27, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28130256/ca2-calmodulin-dependent-protein-kinase-ii%C3%AE-and-ii%C3%AE-mediate-tgf%C3%AE-induced-transduction-of-fibronectin-and-collagen-in-human-pulmonary-fibroblasts
#19
Subhendu Mukherjee, Wei Sheng, Rui Sun, Luke J Janssen
It is now clear that in addition to activating several complex kinase pathways (Smad, MAP kinase, PI3 kinase), TGFβ also acts by elevating [Ca2+] within the cytosol of human pulmonary fibroblasts. Ca2+/calmodulin-dependent protein kinase II (CamK II) is also known to regulate gene expression in fibroblasts. In this study, we examined the interactions between calcium signaling, activation of CamK and other kinases, and extracellular matrix (ECM) gene expression. Human pulmonary fibroblasts were cultured and stimulated with artificially-generated Ca2+-pulses in the absence of TGFβ, or with TGFβ (1 nM) or vehicle in the presence of various blockers of Ca2+ signaling...
January 27, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28104604/hiv-infection-model-of-chronic-obstructive-pulmonary-disease-in-mice
#20
Patrick Geraghty, Eran Hadas, Boe-Hyun Kim, Abdoulaye J Dabo, David J Volsky, Robert Foronjy
Cigarette smoke usage is prevalent in HIV+ patients and, despite highly active antiretroviral therapy (HAART), these individuals develop an accelerated form of chronic obstructive pulmonary disease (COPD). Studies investigating the mechanisms of COPD development in HIV have been limited by the lack of suitable mouse models. Here we describe a model of HIV induced COPD in wild type mice using EcoHIV, a chimeric HIV capable of establishing chronic infection in immunocompetent mice. A/J mice were infected with EcoHIV and subjected to whole body cigarette smoke exposure...
January 19, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
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