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American Journal of Physiology. Lung Cellular and Molecular Physiology

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https://www.readbyqxmd.com/read/29446321/pulmonary-il-1%C3%AE-expression-in-early-life-causes-permanent-changes-in-lung-structure-and-function-in-adulthood
#1
Anna Hogmalm, Maija Bry, Kristina Bry
Chorioamnionitis, mechanical ventilation, oxygen therapy, and postnatal infection promote inflammation in the newborn lung. The long-term consequences of pulmonary inflammation during infancy have not been well characterized. The aim of this study was to examine the impact of inflammation during the late saccular to alveolar stages of lung development on lung structure and function in adulthood. To induce IL-1β expression in the pulmonary epithelium of mice with a tetracycline-inducible human IL-1β transgene, doxycycline was administered via intraperitoneal injections to bitransgenic pups and their littermate controls on postnatal days (PN) 0, 0...
February 15, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29446320/inhibition-of-mucin-secretion-via-glucocorticoid-induced-regulation-of-calcium-related-proteins-in-mouse-lung
#2
Jin Yong An, Changhwan Ahn, Hee Young Kang, Eui-Bae Jeung
Calcium is important for physiological functioning in many tissues and is essential in mucus secretion and muscle contraction. Intracellular concentrations of calcium are regulated by calcium-related proteins such as TRPV4, TRPV6, CaBP-9k, NCX1, and PMCA1. In this study, the relationship between secretion of pulmonary mucus and calcium regulation was investigated. To confirm the effect of steroid hormones, immature mice were injected with estrogen (E2) or progesterone (P4) and mature mice were injected with dexamethasone (DEX)...
February 15, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29417823/drug-induced-pulmonary-arterial-hypertension-a-primer-for-clinicians-and-scientists
#3
Mark E Orcholski, Ke Yuan, Charlotte Rajasingh, Halley Tsai, Elya A Shamskhou, Navneet Kaur Dhillon, Norbert F Voelkel, Roham T Zamanian, Vinicio A de Jesus Perez
Drug-induced pulmonary arterial hypertension (D-PAH) is a form of World Health Organization (WHO) Group 1 pulmonary hypertension (PH) defined by severe small vessel loss and obstructive vasculopathy, which leads to progressive right heart failure and death. To date, 16 different compounds have been associated with D-PAH, including anorexigens, recreational stimulants, and more recently, several Food and Drug Administration (FDA)-approved medications. While the clinical manifestation, pathology, and hemodynamic profile of D-PAH are indistinguishable from other forms of PAH, its clinical course can be unpredictable and to some degree dependent on removal of the offending agent...
February 8, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29417822/go-with-the-back-flow-what-can-retrograde-perfusion-teach-us-about-arterial-remodeling-in-pulmonary-arterial-hypertension
#4
Ketul R Chaudhary, Duncan J Stewart
No abstract text is available yet for this article.
February 8, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29388469/akap1-genetic-deletion-increases-the-severity-of-hyperoxia-induced-acute-lung-injury-in-mice
#5
Venkata R Narala, Jutaro Fukumoto, Helena Hernández-Cuervo, Sahebgowda Sidramagowda Patil, Sudarshan Krishnamurthy, Mason Breitzig, Lakshmi Galam, Ramani Soundararajan, Richard F Lockey, Narasaiah Kolliputi
Critically ill patients are commonly treated with high levels of oxygen, hyperoxia, for prolonged periods of time. Unfortunately, extended exposure to hyperoxia can exacerbate respiratory failure and lead to a high mortality rate. Mitochondrial A-kinase anchoring protein (Akap) has been shown to regulate mitochondrial function. It has been reported that, under hypoxic conditions, Akap121 undergoes proteolytic degradation and promotes cardiac injury. However, the role of Akap1 in hyperoxia-induced acute lung injury (ALI) is largely unknown...
February 1, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29388468/plc%C3%AE-1-pkc%C3%AE%C2%B5-ip3r1-plays-an-important-role-in-hypoxia-induced-calcium-response-in-pulmonary-artery-smooth-muscle-cells
#6
Vishal R Yadav, Tengyao Song, Lin Mei, Leroy Joseph, Yun-Min Zheng, Yong-Xiao Wang
Hypoxia-induced pulmonary vasoconstriction (HPV) is attributed to an increase in intracellular Ca2+ concentration ([Ca2+]i) in pulmonary artery smooth muscle cells (PASMCs). We have reported that phospholipase C-γ1 (PLCγ1) plays a significant role in the hypoxia-induced increase in [Ca2+]i in PASMCs and attendant HPV. In this study, we intended to determine molecular mechanisms for hypoxic Ca2+ and contractile responses in PASMCs. Our data reveal that hypoxic vasoconstriction occurs in PAs, but not in mesenteric arteries (MAs)...
February 1, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29388467/emerging-therapeutics-in-pulmonary-hypertension
#7
Matthew K Hensley, Andrea Levine, Mark T Gladwin, Yen-Chun Lai
Pulmonary hypertension (PH) is a progressive and often fatal illness presenting with nonspecific symptoms of dyspnea, lower extremity edema, and exercise intolerance. Pathologically, endothelial dysfunction leads to abnormal intimal and smooth muscle proliferation along with reduced apoptosis, resulting in increased pulmonary vascular resistance (PVR) and elevated pulmonary pressures. PH is subdivided into five WHO groups based on the disease pathology and specific cause. While there are FDA-approved medications for the treatment of pulmonary arterial hypertension (PAH, Group 1 PH), as well as for chronic thromboembolic pulmonary hypertension (CTEPH, Group 4 PH), the morbidity and mortality remain high...
February 1, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29388466/reactive-oxygen-species-induced-ca2-influx-via-trpv4-and-microvascular-endothelial-dysfunction-in-the-su5416-hypoxia-model-of-pulmonary-arterial-hypertension
#8
Karthik Suresh, Laura Servinsky, Haiyang Jiang, Zahna Bigham, Xin Yun, Corinne Kliment, John C Huetsch, Mahendra Damarla, Larissa A Shimoda
Pulmonary arterial hypertension (PAH) is a lethal disease characterized by elevations in pulmonary arterial pressure, in part due to formation of occlusive lesions in the distal arterioles of the lung. These complex lesions may comprise multiple cell types, including endothelial cells (ECs). To better understand the molecular mechanisms underlying EC dysfunction in PAH, lung microvascular endothelial cells (MVECs) were isolated from normoxic rats (N-MVEC) and rats subjected to SU5416 plus hypoxia (SuHx), an experimental model of PAH...
February 1, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29368550/aurothioglucose-does-not-improve-alveolarization-or-elicit-sustained-nrf2-activation-in-c57bl-6-models-of-bronchopulmonary-dysplasia
#9
Qian Li, Rui Li, Stephanie B Wall, Katelyn Dunigan, Changchun Ren, Tamas Jilling, Lynette K Rogers, Trent E Tipple
We previously showed that the thioredoxin reductase-1 (TrxR1) inhibitor aurothioglucose (ATG) improves alveolarization in hyperoxia-exposed newborn C3H/HeN mice. Our data supported a mechanism by which the protective effects of ATG are mediated via sustained nuclear factor E2-related factor 2 (Nrf2) activation in hyperoxia-exposed C3H/HeN mice 72 h after ATG administration. Given that inbred mouse strains have differential sensitivity and endogenous Nrf2 activation by hyperoxia, the present studies utilized two C57Bl/6 exposure models to evaluate the effects of ATG on lung development and Nrf2 activation...
January 25, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29368549/instillation-of-hyaluronan-reverses-acid-instillation-injury-to-the-mammalian-blood-gas-barrier
#10
Ting Zhou, Zhihong Yu, Ming-Yuan Jian, Israr Ahmad, Carol S Trempus, Brant M Wagener, Jean-Francois Pittet, Saurabh Aggarwal, Stavros Garantziotis, Weifeng Song, Sadis Matalon
Acid (HCl) aspiration during anesthesia may lead to acute lung injury. There is no effective therapy. We hypothesized that HCl, instilled intratracheally in C57BL/6 mice results in the formation of low molecular weight hyaluronan (L-HA), which activates RhoA and ROCK, causing airway hyperresponsiveness (AHR) and increased permeability. Furthermore, instillation of high molecular weight hyaluronan (H-HA; Yabro®), will reverse lung injury. We instilled HCl in C57BL/6 wild type, MPO-/- and CD44-/- mice. WT mice were also instilled intranasally with H-HA (Yabro®) at 1 and 23 h post HCl...
January 25, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29368548/dietary-omega-6-but-not-omega-3-polyunsaturated-or-saturated-fatty-acids-increase-inflammation-in-primary-lung-mesenchymal-cells
#11
Sandra Rutting, Dia Xenaki, Edmund Lau, Jay C Horvat, Lisa G Wood, Philip M Hansbro, Brian G Oliver
Obesity is an important risk factor for developing severe asthma. Dietary fatty acids which are increased in sera of obese individuals and after high fat meals, activate the innate immune system and induce inflammation. This study investigated whether dietary fatty acids directly cause inflammation and/or synergise with obesity-induced cytokines in primary human pulmonary fibroblasts in vitro. Fibroblasts were challenged with BSA-conjugated fatty acids (ω-6 PUFAs, ω-3 PUFAs or SFAs) with or without TNFα and release of the pro-inflammatory cytokines, IL-6 and CXCL8, was measured...
January 25, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29368547/blocking-cxcl1-dependent-neutrophil-recruitment-prevents-pulmonary-damage-and-reduces-rick-of-bacterial-infection-after-inhalation-injury
#12
Julia L Dunn, Laurel B Kartchner, Wesley H Stepp, Lindsey I Glenn, Madison M Malfitano, Samuel Jones, Claire M Doerschuk, Robert Maile, Bruce A Cairns
Smoke inhalation associated with structural fires, wildfires, or explosions leads to lung injury, for which innovative and clinically relevant animal models are needed to develop effective therapeutics. We have previously reported that damage associated molecular patterns (DAMPs) and anti-inflammatory cytokines correlate with infectious complications in patients diagnosed with inhalational injury. In this study, we describe a novel and translational murine model of acute inhalational injury characterized by an accumulation of protein and neutrophils in the bronchoalveolar space, as well as histological evidence of tissue damage...
January 25, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29345200/distinct-niches-within-the-extracellular-matrix-dictate-fibroblast-function-in-cell-free-3d-lung-tissue-cultures
#13
Gerald Burgstaller, Arunima Sengupta, Sarah Vierkotten, Gerhard Preissler, Michael Lindner, Jürgen Behr, Melanie Königshoff, Oliver Eickelberg
Instructive cues from the extracellular matrix (ECM) and their functional interplay with cells play pivotal roles for development, tissue repair, and disease. However, the precise nature of this interplay remains elusive. We used an innovative 3D cell culture ECM model by decellularizing ex vivo lung tissue scaffolds (d3D-LTCs) derived from diseased and healthy mouse lungs, which widely mimics the native (patho)physiological in vivo microenvironment. We successfully repopulated all d3D-LTCs with primary human and murine fibroblasts...
January 18, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29345199/pulmonary-vascular-dysfunction-secondary-to-pulmonary-arterial-hypertension-insights-gained-through-retrograde-perfusion
#14
Chun Zhou, Edward S Crockett, Lynn Batten, Ivan F McMurtry, Troy Stevens
Here, we tested the hypothesis that severe pulmonary arterial hypertension impairs retrograde perfusion. To test this hypothesis, pulmonary arterial hypertension was induced in Fischer rats using a single injection of Sugen 5416 followed by 3 weeks of exposure to 10% hypoxia and then 2 weeks of normoxia. This Sugen 5416 and hypoxia regimen caused severe pulmonary arterial hypertension, with a Fulton Index of 0.73+0.07, reductions in both the pulmonary arterial acceleration time and pulmonary arterial acceleration to pulmonary arterial ejection times ratio, and extensive medial hypertrophy and occlusive neointimal lesions...
January 18, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29345198/fibrin-turnover-and-organization-of-pleural-injury-bench-to-bedside
#15
Andrey A Komissarov, Najib M Rahman, Yc Gary Lee, Galina Florova, Sreerama Shetty, Richard Idell, Mitsuo Ikebe, Kumuda Das, Torry A Tucker, Steven Idell
Recent studies have shed new light on the role of the fibrinolytic system in the pathogenesis of pleural organization, including mechanisms by which the system regulates mesenchymal transition of mesothelial cells and how that process affects outcomes of pleural injury. The key contribution of plasminogen activator inhibitor-1 to the outcomes of pleural injury is now better understood as is its role in the regulation of intrapleural fibrinolytic therapy. In addition, mechanisms by which fibrinolysins are processed after intrapleural administration have now been elucidated, informing new candidate diagnostics and therapeutics for pleural loculation and failed drainage...
January 18, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29345197/neonatal-hyperoxia-depletes-pulmonary-vein-cardiomyocytes-in-adult-mice-via-mitochondrial-oxidation
#16
Min Yee, Ethan David Cohen, William Domm, George A Porter, Andrew N McDavid, Michael A O'Reilly
Supplemental oxygen given to preterm infants has been associated with permanently altering postnatal lung development. Now that these individuals are reaching adulthood, there is growing concern that early-life oxygen exposure may also promote cardiovascular disease through poorly understood mechanisms. We previously reported that adult mice exposed to 100% oxygen between postnatal days 0-4 develop pulmonary hypertension defined pathologically by capillary rarefaction, dilation of arterioles and veins, cardiac failure, and a reduced lifespan...
January 18, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29345196/surfactant-protein-c-dampens-inflammation-by-decreasing-jak-stat-activation-during-lung-repair
#17
Huiyan Jin, Andrzej K Ciechanowicz, Alanna R Kaplan, Lin Wang, Ping Xia Zhang, Yi-Chien Lu, Rachel E Tobin, Brooke A Tobin, Lauren Cohn, Caroline J Zeiss, Patty J Lee, Emanuela M Bruscia, Diane S Krause
Surfactant Protein C (SPC), a key component of pulmonary surfactant, also plays a role in regulating inflammation. SPC deficiency in patients and mouse models is associated with increased inflammation and delayed repair, but the key drivers of SPC-regulated inflammation in response to injury are largely unknown. This study focuses on a new mechanism of SPC as an anti-inflammatory molecule using SPC-TK/SPC-KO (surfactant protein C-thymidine kinase/surfactant protein C knockout) mice, which represent a novel sterile injury model that mimics clinical acute respiratory distress syndrome (ARDS)...
January 18, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29345195/mitochondrial-dysfunction-and-pulmonary-hypertension-cause-effect-or-both
#18
Jeffrey D Marshall, Isabel Bazan, Yi Zhang, Wassim H Fares, Patty J Lee
Pulmonary hypertension describes a heterogeneous disease defined by increased pulmonary artery pressures, and progressive increase in pulmonary vascular resistance due to pathologic remodeling of the pulmonary vasculature involving pulmonary endothelial cells, pericytes, and smooth muscle cells.  This process occurs under various conditions, and though these populations vary, the clinical manifestations are the same: progressive dyspnea, increases in right ventricular (RV) afterload and dysfunction, RV-pulmonary artery uncoupling, and right-sided heart failure with systemic circulatory collapse...
January 18, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29345194/transient-stretch-induces-cytoskeletal-fluidization-through-the-severing-action-of-cofilin
#19
Bo Lan, Ramaswamy Krishnan, Chan Y Park, Rodrigo Watanabe, Ronald Panganiban, James P Butler, Quan Lu, William C Cole, Jeffrey J Fredberg
With every deep inspiration (DI) or sigh the airway wall stretches, as do the airway smooth muscle cells that it contains. In response, the airway smooth muscle (ASM) cell undergoes rapid stretch-induced cytoskeletal fluidization. As a molecular mechanism underlying that ASM fluidization response, here we demonstrate a key role for the actin-severing protein, cofilin. Using primary human ASM cells, we simulated a DI by imposing a transient stretch of physiologic magnitude and duration. We measured the resulting changes in contractile forces using traction microscopy...
January 18, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29345193/serotonin-2a-receptor-inhibition-protects-against-the-development-of-pulmonary-hypertension-and-pulmonary-vascular-remodeling-in-neonatal-mice
#20
Cassidy Delaney, Laurie Sherlock, Susan Fisher, Joanne K Maltzahn, Clyde J Wright, Eva Nozik-Grayck
Pulmonary hypertension (PH) complicating bronchopulmonary dysplasia (BPD) worsens clinical outcomes in former preterm infants. Increased serotonin (5-hydroxytryptamine, 5-HT) signaling plays a prominent role in PH pathogenesis and progression in adults. We hypothesized that increased 5-HT signaling contributes to the pathogenesis of neonatal PH complicating BPD and neonatal lung injury. Thus, we interrogated 5-HT signaling in neonatal mice exposed to bleomycin, previously demonstrated to induce PH and alveolar simplification...
January 18, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
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