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American Journal of Physiology. Lung Cellular and Molecular Physiology

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https://www.readbyqxmd.com/read/28642262/arterial-stiffness-induces-remodeling-phenotypes-in-pulmonary-artery-smooth-muscle-cells-via-yap-taz-mediated-repression-of-cyclooxygenase-2
#1
Paul B Dieffenbach, Christina Mallarino Haeger, Anna Maria F Coronata, Kyoung Moo Choi, Xaralabos Varelas, Daniel J Tschumperlin, Laura E Fredenburgh
Pulmonary arterial stiffness is an independent risk factor for mortality in pulmonary hypertension (PH), and plays a critical role in PH pathophysiology. We have recently demonstrated arterial stiffening early in experimental PH, along with evidence for a mechanobiologic feedback loop by which arterial stiffening promotes further cellular remodeling behaviors. Cyclooxygenase-2 (COX-2) and prostaglandin signaling have been implicated in stiffness-mediated regulation, with prostaglandin activity inversely correlated to matrix stiffness and remodeling behaviors in vitro, as well as to disease progression in rodent PH models...
June 22, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28642261/transforming-growth-factor-beta-stimulates-smad1-5-signaling-in-pulmonary-artery-smooth-muscle-cells-and-fibroblasts-of-the-newborn-mouse-through-alk1
#2
Huili Zhang, Lili Du, Ying Zhong, Kathleen C Flanders, Jesse D Roberts
The intracellular signaling mechanisms through which TGFβ regulates pulmonary development are incompletely understood. Canonical TGFβ signaling involves Smad2/3 phosphorylation, Smad2/3·Smad4 complex formation and nuclear localization, and gene regulation. Here we show that physiologically relevant TGFβ1 levels also stimulate Smad1/5 phosphorylation, typically a mediator of bone morphogenetic protein (BMP) signaling, in mouse pup pulmonary artery smooth muscle cells (mPASMC) and lung fibroblasts and other interstitial lung cell lines...
June 22, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28642260/cigarette-smoke-disrupts-monolayer-integrity-by-altering-epithelial-cell-cell-adhesion-and-cortical-tension
#3
Kristine Nishida, Kieran A Brune, Nirupama Putcha, Pooja Mandke, Wanda K O'Neal, Danny Shade, Vasudha Srivastava, Menghen Wang, Hong Lam, Steven S An, M Bradley Drummond, Nadia N Hansel, Douglas N Robinson, Venkataramana K Sidhaye
Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality. Cigarette smoke (CS) drives disease development and progression. The epithelial barrier is damaged by CS with increased monolayer permeability. However, the molecular changes that cause this barrier disruption and the interaction between adhesion proteins and the cytoskeleton are not well defined. We hypothesized that CS alters monolayer integrity by increasing cell contractility and decreasing cell adhesion in epithelia...
June 22, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28619762/impaired-tnf-tnfr2-signaling-enhances-th2-and-th17-polarization-and-aggravates-allergic-airway-inflammation
#4
Xiao-Ming Li, Xi Chen, Wen Gu, Yi-Jia Guo, Yi Cheng, Juan Peng, Xue-Jun Guo
CD4+T cell differentiation plays an important role in allergic airway diseases. Tumor necrosis factor receptor 2 (TNFR2) has been shown to regulate CD4+T lymphocyte differentiation, but its role in allergic airway inflammation is not clear. Here we investigated the role of TNFR2 in allergic airway inflammation. Mouse model was generated by immunization with OVA and intranasal administration of TNFR2 antibody. Airway inflammation and CD4+T cell differentiation were measured in vivo and in vitro. Inhibited TNFR2 signaling aggravated airway inflammation and increased the expression of inflammatory cytokines (IL-4, IL-5, IL-17, and TNF-α) in serum and bronchoalveolar lavage fluid (BALF)...
June 15, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28619761/exhaled-breath-condensate-biomarkers-for-the-early-diagnosis-of-lung-cancer-using-proteomics
#5
Laura M López-Sánchez, Bernabé Jurado-Gámez, Nuria Feu-Collado, Araceli Valverde, Amanda Cañas, Jose L Fernández-Rueda, Enrique Aranda, Antonio Rodríguez-Ariza
We explored whether the proteomic analysis of exhaled breath condensate (EBC) may provide biomarkers for non-invasive screening for the early detection of lung cancer (LC). EBC was collected from 192 individuals (49 control (C), 49 risk factor-smoking (S), 46 chronic obstructive pulmonary disease (COPD) and 48 LC (LC)). Using LC-MS/MS, 348 different proteins with a different pattern among the four groups were identified in EBC samples. Significantly more proteins were identified in the EBC from LC compared to other groups (C:12...
June 15, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28596295/genetic-variance-is-associated-with-susceptibility-for-cigarette-smoke-induced-damp-release-in-mice
#6
Simon D Pouwels, Alen Faiz, Lisette E den Boef, Reneé Gras, Maarten van den Berge, H Marike Boezen, Ron Korstanje, Nick H T Ten Hacken, Antoon J M van Oosterhout, Irene H Heijink, Martijn C Nawijn
Chronic obstructive pulmonary disease (COPD) is characterized by unresolved neutrophilic airway inflammation, and is caused by chronic exposure to toxic gases, such as cigarette smoke (CS), in genetically susceptible individuals. Recent data indicate a role for Damage Associated Molecular Patterns (DAMPs) in COPD. Here, we investigated the genetics of CS-induced DAMP release in 28 inbred mouse strains. Subsequently, in lung tissue from a subset of strains the expression of the identified candidate genes was analyzed...
June 8, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28596294/the-metalloproteinase-adam8-promotes-leukocyte-recruitment-in-vitro-and-in-acute-lung-inflammation
#7
Daniela Dreymueller, Jessica Pruessmeyer, Julian Schumacher, Sandra Fellendorf, Franz Martin Hess, Anke Seifert, Aaron Babendreyer, Joerg Walter Bartsch, Andreas Ludwig
Alveolar leukocyte recruitment is a hallmark of acute lung inflammation and involves transmigration of leukocytes through endothelial and epithelial layers. The disintegrin and metalloproteinase (ADAM) 8 is expressed on human isolated leukocytic cells and can be further upregulated on cultured endothelial and epithelial cells by proinflammatory cytokines. By shRNA mediated knockdown we show that leukocytic ADAM8 is required on monocytic THP-1 cells for chemokine-induced chemotaxis as well as transendothelial and transepithelial migration...
June 8, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28596293/the-uncoupling-of-autophagy-and-zinc-homeostasis-in-airway-epithelial-cells-as-a-fundamental-contributor-to-copd
#8
Eugene Roscioli, Hai Bac Tran, Hubertus Jersmann, Phan Tien Nguyen, Emily Hopkins, Susan Elizabeth Lester, Nigel Farrow, Peter D Zalewski, Paul N Reynolds, Sandra Hodge
The proper regulation of Zinc (Zn) trafficking proteins and the cellular distribution of Zn is critical for the maintenance of autophagic processes. However, there have been no studies which have examined Zn dyshomeostasis and the disease-related modulation of autophagy observed in the airways afflicted with COPD. We hypothesized that dysregulated autophagy in airway epithelial cells (AEC) is related to Zn dysregulation in cigarette smoke (CS)-induced COPD. We applied a human ex vivo air-liquid interface model, a murine model of smoke-exposure, and human lung tissues, and investigated Zn, ZIP1 and ZIP2 Zn-influx proteins, autophagy (Microtubule-associated 1A/1B-light chain-3 (LC3), Beclin-1), autophagic flux (Sequestosome), apoptosis (Bcl2; X-Linked Inhibitor of Apoptosis (XIAP), Poly (ADP)-ribose Polymerase (PARP)), and inflammation (TSLP, RANTES, and IL-1β)...
June 8, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28596292/the-pde4-inhibitor-chf-6001-and-lamas-inhibit-bronchoconstriction-induced-remodelling-in-lung-slices
#9
Loes Em Kistemaker, Tjitske A Oenema, Hoeke A Baarsma, I Sophie T Bos, Martina Schmidt, Fabrizio Facchinetti, Maurizio Civelli, Gino Villetti, Reinoud Gosens
Background Combination therapy of PDE4 inhibitors and anticholinergics induces bronchoprotection in COPD. Mechanical forces that arise during bronchoconstriction may contribute to airway remodelling. Therefore, we investigated the impact of PDE4 inhibitors and anticholinergics on bronchoconstriction-induced remodelling. Because of the different mechanism of action of PDE4 inhibitors and anticholinergics, we hypothesized functional interactions of these two drug classes. Methods Guinea pig precision cut lung slices were pre-incubated with the PDE4-inhibitors CHF-6001 or roflumilast and/or the anticholinergics tiotropium or glycopyorrolate, followed by stimulation with methacholine (10 μM) or TGF -β1 (2 ng/mL) for 48 hours...
June 8, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28572155/elastin-receptor-s-gal-occupancy-by-elastin-peptides-modulates-t-cell-response-during-murine-emphysema
#10
Aïda Meghraoui-Kheddar, Alexandre Pierre, Mehdi Sellami, Sandra Audonnet, Flora Lemaire, Richard Le Naour
Chronic obstructive pulmonary disease and emphysema are associated with increased elastin peptides (EP) production due to excessive breakdown of lung connective tissue. We recently reported that exposure of mice to EP elicited hallmark features of emphysema. EP effects are largely mediated through a receptor complex which includes the elastin-binding protein S-gal. In previous studies, we established a correlation between cytokine production and S-gal protein expression in EP treated immune cells. In this study, we investigated the S-gal-dependent EP effects on T helper (Th) and T cytotoxic (Tc) responses during murine EP-triggered pulmonary inflammation...
June 1, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28572154/novel-role-of-npy-in-neuro-immune-interaction-and-lung-growth-after-intrauterine-growth-restriction
#11
Chansutha Thangaratnarajah, Katharina Dinger, Christina Vohlen, Christian Klaudt, Jawed Nawabi, Eva Lopez Garcia, Grazyna Kwapiszewska, Julia Dobner, Kai D Nuesken, Silke van Koningsbruggen-Rietschel, Stephan von Hoersten, Jörg Dötsch, Miguel Angel Alejandre Alcazar
Individuals with intrauterine growth restriction (IUGR) are at risk for chronic lung disease. Using a rat model, our previous studies showed that altered lung structure is related to IL-6/STAT3 signaling. As Neuropeptide Y (NPY), a co-neurotransmitter of the sympathetic nerve system, regulates proliferation and immune response, we hypothesized that dysregulated NPY after IUGR is linked to IL-6, impaired myofibroblast function, and alveolar growth. IUGR was induced in rats by isocaloric low-protein diet; lungs were analyzed on embryonic day (E) 21, postnatal day (P) 3, P12 and P23...
June 1, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28546155/long-term-nicotine-exposure-dampens-lps-induced-nerve-mediated-airway-hyperreactivity-in-murine-airways
#12
Yuan Xu, Lars-Olaf Cardell
Nicotine is a major component of cigarette smoke. It causes addiction and is used clinically to aid smoke cessation. The aim of the present study is to investigate the effect of nicotine on lipopolysaccharide (LPS)-induced airway hyperreactivity (AHR) and to explore the potential involvement of neuronal mechanisms behind nicotine's effects in murine models in vivo and in vitro. BALB/c mice were exposed to nicotine in vivo via subcutaneous Alzet osmotic minipumps containing nicotine tartate salt solution (24 mg/kg/day) for 28 days...
May 25, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28546154/synergistic-mucus-secretion-by-histamine-and-il-4-through-tmem16a-in-airway-epithelium
#13
Ju Wan Kang, Yong Hyuk Lee, Min Jeong Kang, Hyun Jae Lee, Ryung Oh, Hyun Jin Min, Wan Namkung, Jae Young Choi, Sang Nam Lee, Chang-Hoon Kim, Joo-Heon Yoon, Hyung-Ju Cho
Histamine is an important mediator of allergic reactions, and mucus hypersecretion is a major allergic symptom. However, the direct effect of histamine on mucus secretion from airway mucosal epithelia has not been clearly demonstrated. TMEM16A is a Ca2+-activated chloride channel, and it is closely related to fluid secretion in airway mucosal epithelia. We investigated whether histamine directly induces fluid secretion from epithelial cells or submucosal glands (SMG) and mechanisms related therewith in allergic airway diseases...
May 25, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28546153/impact-of-ventilation-induced-lung-injury-on-the-structure-and-function-of-lamellar-bodies
#14
Scott Milos, Reza Khazaee, Lynda A McCaig, Karen Nygard, Richard B Gardiner, Yi Y Zuo, Cory M Yamashita, Ruud A W Veldhuizen
Alterations to the pulmonary surfactant system have been observed consistently in ventilation-induced lung injury including composition changes and impairments in the surface tension reducing ability of the isolated extracellular surfactant. However, there is limited information about the effects of VILI on the intracellular form of surfactant, the lamellar body. It is hypothesized that VILI leads to alterations of lamellar bodies numbers and function. To test this hypothesis, rats were randomized to one of three groups, non-ventilated controls, control ventilation and high tidal volume ventilation (VILI)...
May 25, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28522569/brain-derived-neurotrophic-factor-and-airway-fibrosis-in-asthma
#15
Michelle R Freeman, Venkatachalem Sathish, Logan J Manlove, Shengyu Wang, Rodney D Britt, Michael A Thompson, Christina M Pabelick, Y S Prakash
Airway remodeling in asthma driven by inflammation involves proliferation of epithelial cells and airway smooth muscle (ASM), as well as enhanced extracellular matrix (ECM) generation and deposition, i.e. fibrosis. Accordingly, understanding pro-fibrotic mechanisms is important for developing novel therapeutic strategies in asthma. Recent studies, including our own, have suggested a role for locally-produced growth factors such as brain-derived neurotrophic factor (BDNF) in mediating and modulating inflammation effects...
May 18, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28522568/peroxisome-proliferator-activated-receptor-gamma-enhances-human-pulmonary-artery-smooth-muscle-cell-apoptosis-through-microrna-21-and-programmed-cell-death-4
#16
David Emerson Green, Tamara C Murphy, Bum-Yong Kang, Brahmchetna Bedi, Zhihong Yuan, Ruxana T Sadikot, C Michael Hart
Pulmonary hypertension (PH) is a progressive disorder whose cellular pathogenesis involves enhanced smooth muscle cell (SMC) proliferation and resistance to apoptosis signals. Existing evidence demonstrates that the tumor suppressor, programmed cell death 4 (PDCD4) affects patterns of cell growth and repair responses in the systemic vasculature following experimental injury. In the current study, the regulation PDCD4 and its functional effects on growth and apoptosis susceptibility in pulmonary artery smooth muscle cells was explored...
May 18, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28522567/myeloid-epithelial-crosstalk-coordinates-synthesis-of-the-tissue-protective-cytokine-leukemia-inhibitory-factor-during-pneumonia
#17
Katrina E Traber, Elise M Symer, Eri Allen, Yuri Kim, Kristie L Hilliard, Gregory A Wasserman, Colin L Stewart, Matthew R Jones, Joseph P Mizgerd, Lee Joseph Quinton
In bacterial pneumonia, lung damage resulting from epithelial cell injury is a major contributor to the severity of disease, and in some cases, can lead to long-term sequelae, especially in the setting of severe lung injury or ARDS. Leukemia inhibitory factor (LIF), a member of the IL-6 cytokine family, is a critical determinant of lung tissue protection during pneumonia, but the cellular sources of LIF and the signaling pathways leading to its production in the infected lung are not known. Here, we demonstrate that lung epithelium, specifically alveolar type II cells, is the predominant site of LIF transcript induction in pneumonic mouse lungs...
May 18, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28522566/nedd8-modification-of-cullin-5-regulates-lipopolysaccharide-induced-acute-lung-injury
#18
Ziyan Zhu, Lei Sun, Rui Hao, Hongchao Jiang, Feng Qian, Richard D Ye
Lung infections are major causes of acute lung injury (ALI), with limited effective treatment available. Tumor necrosis factor receptor-associated factor 6 (TRAF6) is an essential adaptor regulating Toll-like receptors (TLRs). We recently identified Cullin-5 (Cul-5) as a prominent component in the regulation of TRAF6 polyubiquitination, but its physiological significance in acute lung injury has not been explored. In this study, we investigated the potential role of Cul-5 in regulating ALI using mice receiving intratracheal instillation of LPS...
May 18, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28522565/integrin-%C3%AE-v%C3%AE-5-inhibition-protects-against-ischemia-reperfusion-induced-lung-injury-in-an-autophagy-dependent-manner
#19
Dan Zhang, Chichi Li, Yuanlin Song, Jian Zhou, Yuping Li, Jing Li, Chunxue Bai
Integrin αvβ5 mediates pulmonary endothelial barrier function and acute lung injury (LI), but its roles in cell apoptosis and autophagy are unclear. Thus, the aims of this study were to investigate the significance of αvβ5 in ischemia/reperfusion (I/R)-induced apoptosis and LI and to explore the relationship between αvβ5 and autophagy. Human pulmonary micro-vascular endothelial cells (HPMVECs) were pretreated with an αvβ5-blocking antibody (ALULA) and challenged with oxygen-glucose deprivation/oxygen-glucose restoration, which mimics I/R; then, cellular autophagy and apoptosis were detected, and cell permeability was assessed...
May 18, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28522564/decreased-phosphatase-pten-amplifies-pi3k-signaling-and-enhances-pro-inflammatory-cytokine-release-in-copd
#20
Satoru Yanagisawa, Jonathan R Baker, Chaitanya Vuppusetty, Peter Fenwick, Louise E Donnelly, Kazuhiro Ito, Peter J Barnes
The phosphatidylinositol 3-kinase (PI3K) pathway is activated in chronic obstructive pulmonary disease (COPD), but the regulatory mechanisms for this pathway are yet to be elucidated. Our aim was to determine the expression and role of phosphatase and tensin homolog deleted from chromosome 10 (PTEN), a negative regulator of the PI3K pathway, in COPD. PTEN expression and activity were measured in the peripheral lung of COPD patients compared to smoking and non-smoking controls. The direct influence of cigarette smoke extract (CSE) on PTEN expression was assessed using primary lung epithelial cells and a cell line (BEAS-2B) in the presence or absence of L-buthionine-sulfoximine (BSO) to deplete intracellular glutathione...
May 18, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
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