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American Journal of Respiratory Cell and Molecular Biology

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https://www.readbyqxmd.com/read/30633545/growth-differentiation-factor-gdf-15-in-pulmonary-and-critical-care-medicine
#1
Fien M Verhamme, Christine M Freeman, Guy G Brusselle, Ken R Bracke, Jeffrey L Curtis
Growth differentiation factor 15 (GDF-15) acts both as a stress-induced cytokine with diverse actions at different body sites and as a cell-autonomous regulator linked to cellular senescence and apoptosis. For multiple reasons, this divergent transforming growth factor (TGF)-β molecular superfamily member should be better known to pulmonary researchers and clinicians. In ambulatory individuals, GDF-15 concentrations in peripheral blood are an established predictive biomarker of all-cause mortality and of adverse cardiovascular events...
January 11, 2019: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30620615/ovine-models-of-congenital-heart-disease-and-the-consequences-of-hemodynamic-alterations-for-pulmonary-artery-remodeling
#2
Rebecca Johnson Kameny, Sanjeev A Datar, Jason B Boehme, Catherine Morris, Terry Zhu, Brian D Goudy, Eric G Johnson, Csaba Galambos, Gary W Raff, Xutong Sun, Ting Wang, Samuel R Chiacchia, Qing Lu, Stephen M Black, Emin Maltepe, Jeffrey R Fineman
The natural history of pulmonary vascular disease (PVD) associated with congenital heart disease (CHD) depends upon associated hemodynamics. Patients exposed to increased pulmonary blood flow (PBF) and pulmonary arterial pressure (PAP) develop PVD more commonly than patients exposed to increased PBF alone. To investigate the effects of these differing mechanical forces on physiologic and molecular responses, we developed two models of CHD utilizing fetal surgical techniques: 1) left pulmonary artery (LPA) ligation primarily resulting in increased PBF; and 2) aortopulmonary shunt placement resulting in increased PBF and PAP...
January 8, 2019: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30608868/il-17a-producing-%C3%AE-%C3%AE-t-cells-inhibit-the-formation-of-malignant-pleural-effusions
#3
Xiao-Shan Wei, Xue-Bin Pei, Ya-Lan Liu, Xiu-Zhi Wu, Huan-Zhong Shi, Qiong Zhou
γδT cells are an important source of IL-17A and play an anti- or pro-tumor role depending on the surrounding microenvironment. The precise role of γδT cells in the development of malignant pleural effusions (MPE) remains unknown. Using flow cytometry, the distribution and differentiation of γδT cells in wild-type (WT) and IL-10-⁄- mice were analyzed. The influence of γδT cells on the formation of MPE was carefully elucidated by depleting γδT cells from WT, IL-10-⁄-, and IL-17a-⁄- mice. The distribution of γδT17 cells in human MPE and peripheral blood was also determined...
January 4, 2019: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30608861/stat3-regulates-the-onset-of-oxidant-induced-senescence-in-lung-fibroblasts
#4
David W Waters, Kaj E C Blokland, Prabuddha S Pathinayake, Lan Wei, Michael Schuliga, Jade Jaffar, Glen P Westall, Philip M Hansbro, Cecilia M Prele, Steven E Mutsaers, Nathan W Bartlett, Janette K Burgess, Christopher L Grainge, Darryl A Knight
Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease of unknown cause with a median survival of only 3 years. We and others have shown that fibroblasts derived from IPF-lungs display characteristics of senescent cells and that dysregulated activation of the transcription factor signal transducer and activator of transcription 3 (STAT3) correlates with IPF progression. The question of whether STAT3 activation is involved in fibroblast senescence remains unanswered. We hypothesized that inhibiting STAT3 activation after oxidant-induced senescence would attenuate characteristics of the senescent phenotype...
January 4, 2019: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30605348/myocardin-is-involved-in-mesothelial-mesenchymal-transition-of-human-pleural-mesothelial-cells
#5
Torry Tucker, Yoshikazu Tsukasaki, Tsuyoshi Sakai, Shinya Mitsuhashi, Satoshi Komatsu, Ann Jeffers, Steven Idell, Mitsuo Ikebe
Pleural fibrosis is characterized by severe inflammation of the pleural space, pleural reorganization. Subsequent thickening of visceral pleura contributes to lung stiffness and impaired lung function. Pleural mesothelial cells (PMCs) can become myofibroblasts via mesothelial-mesenchymal transition (MesoMT) and contribute to pleural organization, fibrosis and rind formation. However, mechanisms that underlie MesoMT remain unclear. Here, we investigated the role of myocardin in the induction of MesoMT. TGF-β and thrombin induce MesoMT and markedly upregulated myocardin expression but not myocardin related transcription factors (MRTF)-A and -B in human PMCs (HPMCs)...
January 3, 2019: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30576224/old-cells-in-young-airway-smooth-muscle-does-neonatal-senescence-cause-lifelong-airway-obstruction
#6
Sarah K Sasse, Anthony N Gerber
No abstract text is available yet for this article.
December 21, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30576223/the-club-cell-marker-scgb1a-downstream-of-foxa1-is-reduced-in-asthma
#7
Lingxiang Zhu, Lingling An, Di Ran, Rosa Lizarraga, Cheryl Bondy, Xu Zhou, Richart W Harper, Shu-Yi Liao, Yin Chen
Human SCGB1A1 protein has been shown to be significantly reduced in bronchoalveolar lavage, sputum and serum from human asthmatics as compared to healthy individuals. However, the mechanism of this reduction and its functional impact have not been entirely elucidated. By mining online datasets, we found that the message RNA of SCGB1A1 was significantly repressed in brushed human airway epithelial cells from asthmatics and this repression appeared to be associated with the reduced expression of FOXA2. Consistently, both Scgb1A1 and FoxA2 were downregulated in an ovalbumin (OVA)-induced mouse model of asthma...
December 21, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30576219/vaporized-e-cigarette-liquids-induce-ion-transport-dysfunction-in-airway-epithelia
#8
Vivian Y Lin, Matthew D Fain, Patricia L Jackson, Taylor F Berryhill, Landon S Wilson, Marina Mazur, Stephen J Barnes, J Edwin Blalock, S Vamsee Raju, Steven M Rowe
Cigarette smoking is associated with chronic obstructive pulmonary disease and chronic bronchitis. Acquired ion transport abnormalities, including CFTR dysfunction, caused by cigarette smoking have been proposed as potential mechanisms for mucus obstruction in chronic bronchitis. Although popular and perceived to be safe, it remains unclear if e-cigarette use harms the airways via mechanisms altering ion transport. Here, we sought to determine if e-cigarette vapor, like cigarette smoke, had the potential to induce acquired CFTR dysfunction, and to what degree...
December 21, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30571144/fatty-acid-oxidation-protects-against-hyperoxia-induced-endothelial-cell-apoptosis-and-lung-injury-in-neonatal-mice
#9
Hongwei Yao, Jiannan Gong, Abigail L Peterson, Xuexin Lu, Peng Zhang, Phyllis A Dennery
In neonates, hyperoxia or positive pressure ventilation causes continued lung injury characterized by simplified vascularization and alveolarization, which are the hallmarks of bronchopulmonary dysplasia. Although endothelial cells (ECs) have metabolic flexibility to maintain cell function under stress, it is unknown whether hyperoxia causes metabolic dysregulation in ECs, leading to lung injury. We hypothesized that hyperoxia alters EC metabolism, which causes EC dysfunction and lung injury. To test this hypothesis, we exposed lung ECs to hyperoxia (95% O2/5% CO2) followed by air recovery (O2/rec)...
December 20, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30571141/emphysema-associated-autoreactive-antibodies-exacerbate-post-lung-transplant-ischemia-reperfusion-injury
#10
Kunal J Patel, Qi Cheng, Sarah Stephenson, D Patterson Allen, Changhai Li, Jane Kilkenny, Ryan Finnegan, Valeria Montalvo-Calero, Scott Esckilsen, Chentha Vasu, Martin Goddard, Satish N Nadig, Carl Atkinson
COPD-associated chronic inflammation has been shown to lead to an autoimmune phenotype characterized in part by the presence of lung reactive autoreactive antibodies. We hypothesized that ischemia reperfusion injury (IRI) liberates epitopes that would facilitate pre-existing autoantibody binding, thereby exacerbating lung injury post-transplantation. We induced emphysema in C57BL/6 mice through 6 months of cigarette smoke exposure (CS). CS exposure significantly elevated serum autoantibodies compared to non-smoke age-matched (NS) mice...
December 20, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30571139/pulmonary-neuroendocrine-cells-secrete-gaba-to-induce-goblet-cell-hyperplasia-in-primate-models
#11
Juliana Barrios, Alvin T Kho, Linh Aven, Jennifer A Mitchel, Jin-Ah Park, Scott H Randell, Lisa A Miller, Kelan G Tantisira, Xingbin Ai
Mucus overproduction is a major contributor to morbidity and mortality in asthma. Mucus overproduction is induced by orchestrated actions of multiple factors that include inflammatory cytokines and γ-aminobutyric acid (GABA). GABA is produced only by pulmonary neuroendocrine cells (PNECs) in the mouse lung. Recent studies in a neonatal mouse model of allergic inflammation have shown that PNECs play an essential role in mucus overproduction by GABA hypersecretion. Whether PNECs mediate dysregulated GABA signaling for mucus overproduction in asthma is unknown...
December 20, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30562054/lung-adenocarcinoma-syndecan-2-potentiates-cell-invasiveness
#12
Konstantin Tsoyi, Juan C Osorio, Sarah G Chu, Isis E Fernandez, Sergio Poli, Lynette Sholl, Ye Cui, Carmen S Tellez, Jill M Siegfried, Steven A Belinsky, Mark A Perrella, Souheil El-Chemaly, Ivan O Rosas
RATIONALE: Altered expression of syndecan-2, a heparan sulfate proteoglycan, has been associated with diverse types of human cancers. However, the mechanisms by which syndecan-2 may contribute to the pathobiology of lung adenocarcinoma have not been previously explored. METHODS: Syndecan-2 levels were measured in human lung adenocarcinoma samples and Lung Cancer Tissue Microarrays using immunohistochemistry and real time-PCR. To understand the role of syndecan-2 in vitro, SDC2 was silenced or overexpressed in A549 lung adenocarcinoma cells...
December 18, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30562052/stretch-activated-piezo1-channel-in-endothelial-cells-relaxes-mouse-intrapulmonary-arteries
#13
Audrey Lhomme, Guillaume Gilbert, Thomas Pele, Juliette Deweirdt, Daniel Henrion, Isabelle Baudrimont, Marilyne Campagnac, Roger Marthan, Christelle Guibert, Thomas Ducret, Jean-Pierre Savineau, Jean-François Quignard
In intrapulmonary artery (IPA), endothelial cells (EC) respond to mechanical stimuli by releasing vasoactive factors to set the vascular tone. Piezo1, a stretch-activated calcium permeable channel is a sensor of mechanical stress in EC. The present study was undertaken to investigate the implication of Piezo1 in the endothelium-dependent regulation of IPA tone and its potential involvement in pulmonary hypertension, the main disease of this circulation. IPA tone was quantified by means of a myograph in control Piezo1+/+ mouse and in mouse lacking endothelial Piezo1 (EC-Piezo1-/-)...
December 18, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30562051/oxygen-disrupts-human-fetal-lung-mesenchymal-cells-implications-for-bronchopulmonary-dysplasia
#14
Marius A Möbius, Daniel Freund, Arul Vadivel, Sarah Koss, Suzanne McConaghy, Robin K Ohls, Mario Rüdiger, Bernard Thébaud
RATIONALE AND OBJECTIVES: Exogenous mesenchymal stromal cells ameliorate experimental bronchopulmonary dysplasia. Moreover, data from term-born animal models and human tracheal aspirate-derived cells suggests altered mesenchymal signaling pathways in the pathophysiology of neonatal lung disease. Here, we sought to determine if tissue-resident human fetal lung mesenchymal cells contribute to normal and oxygen-impaired lung development, thus linking endogenous mesenchymal (dys-)function and exogenous mesenchymal cell repair activity...
December 18, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30562049/-yap-ing-about-the-antifibrotic-benefits-of-prostacyclin
#15
Steven K Huang
No abstract text is available yet for this article.
December 18, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30562048/advancing-copd-therapy-opportunities-challenges-and-excitement
#16
Stephen I Rennard
No abstract text is available yet for this article.
December 18, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30562042/systems-analysis-of-the-human-pulmonary-arterial-hypertension-lung-transcriptome
#17
Robert S Stearman, Quan M Bui, Gil Speyer, Adam Handen, Amber R Cornelius, Brian B Graham, Seungchan Kim, Elizabeth A Mickler, Rubin M Tuder, Stephen Y Chan, Mark W Geraci
RATIONALE: Pulmonary arterial hypertension (PAH) is characterized by increased pulmonary artery pressure and vascular resistance, typically leading to right heart failure and death. Current therapies improve quality of life of the patients but have a modest effect on long-term survival. A detailed transcriptomics and systems biology view of the PAH lung is expected to provide new testable hypotheses for exploring novel treatments. OBJECTIVES: Complete transcriptomics analysis of PAH and control lung tissue to develop disease-specific and clinical data/tissue pathology gene expression classifiers from expression datasets...
December 18, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30543447/intracellular-heat-shock-protein-70-deficiency-in-pulmonary-fibrosis
#18
Jacobo Sellares, Kristen L Veraldi, Katelynn J Thiel, Nayra Cárdenes, Diana Alvarez, Frank Schneider, Joseph M Pilewski, Mauricio Rojas, Carol A Feghali-Bostwick
Idiopathic Pulmonary Fibrosis (IPF) pathogenesis has been postulated to involve a variety of mechanisms associated with the aging process, including loss of protein homeostasis (proteostasis). Heat shock proteins (Hsp) are cellular chaperones that serve a number of vital maintenance and repair functions, including the regulation of proteostasis. Previously published data have implicated Hsp70 in the development of pulmonary fibrosis in animal models. We sought to identify alterations in Hsp70 expression in IPF lung...
December 13, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30540914/another-weapon-in-the-battle-against-idiopathic-pulmonary-fibrosis
#19
Carole L Wilson, Chi F Hung
No abstract text is available yet for this article.
December 12, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30540913/the-tyrosine-kinase-inhibitor-tas-115-attenuates-bleomycin-induced-lung-fibrosis-in-mice
#20
Kazuya Koyama, Hisatsugu Goto, Shun Morizumi, Kozo Kagawa, Haruka Nishimura, Seidai Sato, Hiroshi Kawano, Yuko Toyoda, Hirohisa Ogawa, Sakae Homma, Yasuhiko Nishioka
The signaling pathways of growth factors including platelet-derived growth factor (PDGF) can be considered specific targets for overcoming the poor prognosis of idiopathic pulmonary fibrosis (IPF). Nintedanib, the recently approved multiple kinase inhibitor, has shown promising anti-fibrotic effects in IPF patients; however, its efficacy is still limited, and in some cases, treatment discontinuation is necessary due to toxicities such as gastrointestinal disorders. Therefore, more effective agents with less toxicity are still needed...
December 12, 2018: American Journal of Respiratory Cell and Molecular Biology
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