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American Journal of Physiology. Lung Cellular and Molecular Physiology

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https://www.readbyqxmd.com/read/29212803/elastase-alters-contractility-and-promotes-an-inflammatory-synthetic-phenotype-in-airway-smooth-muscle-tissues
#1
Angelia D Lockett, Yidi Wu, Susan J Gunst
Neutrophil elastase is secreted by inflammatory cells during airway inflammation and can elicit airway hyperactivity in vivo. Elastase can degrade multiple components of the extracellular matrix. We hypothesized that elastase might disrupt the connections between airway smooth muscle (ASM) cells and the extracellular matrix, and that this might have direct effects on ASM tissue responsiveness and inflammation. The effect of elastase treatment on ASM contractility was assessed in vitro in isolated strips of canine tracheal smooth muscle by stimulating tissues with cumulatively increasing concentrations of ACh and measuring contractile force...
December 6, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29212802/transcriptional-survey-of-alveolar-macrophages-in-a-murine-model-of-chronic-granulomatous-inflammation-reveals-common-themes-with-human-sarcoidosis
#2
Arjun Mohan, Anagha Malur, Matthew McPeek, Barbara P Barna, Lynn M Schnapp, Mary Jane Thomassen, Sina A Gharib
To advance our understanding of the pathobiology of sarcoidosis, we developed a multiwall carbon nanotube (MWCNT)-based murine model that shows marked histological and inflammatory signal similarities to this disease. In this study, we compared the alveolar macrophage transcriptional signatures of our animal model with human sarcoidosis to identify overlapping molecular programs. Whole-genome microarrays were used to assess gene expression of alveolar macrophages in 6 MWCNT-exposed and 6 control animals. The results were compared to the transcriptional profiles of alveolar immune cells in 15 sarcoidosis patients and 12 healthy humans...
December 6, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29212801/roles-of-high-mobility-group-box-1-and-thrombin-in-murine-pulmonary-fibrosis-and-the-therapeutic-potential-of-thrombomodulin
#3
Takashi Kida, Takahiro Seno, Hidetake Nagahara, Takuya Inoue, Amane Nakabayashi, Yuji Kukida, Kazuki Fujioka, Wataru Fujii, Makoto Wada, Masataka Kohno, Yutaka Kawahito
Cross-talk between inflammation and coagulation plays important roles in acute or subacute progressive pulmonary fibrosis characterized by diffuse alveolar damage. Thrombomodulin is a physiological inhibitor of high-mobility group box 1 (HMGB1) and thrombin, and may be effective for this condition. This study investigated the roles of HMGB1 and thrombin in the pathophysiology of bleomycin-induced pulmonary fibrosis and the efficacy of recombinant human soluble thrombomodulin (rhTM). Pulmonary fibrosis was induced in wild-type C57BL/6 mice by intratracheal instillation of bleomycin...
December 6, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29212800/extracellular-retention-of-pdgf-b-directs-vascular-remodeling-in-mouse-hypoxia-induced-pulmonary-hypertension
#4
Philip Tannenberg, Ya-Ting Chang, Lars Muhl, Bàrbara Laviña, Hanna Gladh, Guillem Genové, Christer Betsholtz, Erika Folestad, Karin Tran-Lundmark
Pulmonary hypertension (PH) is a lethal condition and current vasodilator therapy has limited effect. Anti-proliferative strategies targeting platelet-derived growth factor (PDGF) receptors, such as imatinib, have generated promising results in animal studies. Imatinib is however a non-specific tyrosine kinase inhibitor and has in clinical studies caused unacceptable adverse events. Further studies are needed on the role of PDGF signaling in PH. Here, mice expressing a variant of PDGF-B with no retention motif (Pdgfbret/ret), resulting in defective binding to extracellular matrix, were studied...
December 6, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29192094/over-production-of-growth-differentiation-factor-15-gdf15-promotes-human-rhinovirus-infection-and-virus-induced-inflammation-in-the-lung
#5
Qun Wu, Di Jiang, Niccolette R Schaefer, Laura Harmacek, Brian P O'Connor, Thomas Eling, Oliver Eickelberg, Hong Wei Chu
Human rhinovirus (HRV) is the most common virus contributing to acute exacerbations of chronic obstructive pulmonary disease (COPD) nearly year-round, but the mechanisms have not been well elucidated. Recent clinical studies suggest that high levels of growth differentiation factor 15 (GDF15) protein in the blood are associated with an increased yearly rate of all-cause COPD exacerbations. Therefore, in the current study, we investigated whether GDF15 promotes HRV infection and virus-induced lung inflammation...
November 30, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29167126/chronic-lung-injury-and-impaired-pulmonary-function-in-a-mouse-model-of-acid-ceramidase-deficiency
#6
Fabian Ps Yu, Diana Islam, Jakub Sikora, Shaalee Dworski, Jiří Gurka', Lucia Lopez-Vasquez, Mingyao Liu, Wolfgang Michael Kuebler, Thierry Levade, Haibo Zhang, Jeffrey A Medin
Farber Disease (FD) is a debilitating Lysosomal Storage Disorder (LSD) caused by a deficiency of acid ceramidase (ACDase) activity due to mutations in the gene ASAH1. Patients with ACDase deficiency may develop a spectrum of clinical phenotypes. Severe cases of FD are frequently associated with neurological involvement, failure to thrive, and respiratory complications. Mice homozygous (Asah1P361R/P361R) for an orthologous patient mutation in Asah1 recapitulate human FD. In this study, we show significant impairment in lung function including low compliance and increased airway resistance in a mouse model of ACDase deficiency...
November 22, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29167125/mesenchymal-stem-cells-reduce-hypoxia-induced-apoptosis-in-alveolar-epithelial-cells-by-modulating-hif-and-ros-hypoxic-signalings
#7
Olivier Bernard, Florence Jeny, Yurdagul Uzunhan, Elisabetta Dondi, Rahma Terfous, Rabab Label, Angela Sutton, Jérôme Larghero, Valérie Vanneaux, Hilario Nunes, Emilie Boncoeur, Carole Planès, Nicolas Dard
Distal lung diseases such as pulmonary fibrosis or acute lung injury are commonly associated with local alveolar hypoxia that may be deleterious through the stimulation of alveolar epithelial cell (AEC) apoptosis. In various murine models of alveolar injury, administration of allogenic human mesenchymal stem cells (hMSC) exerts an overall protective paracrine effect limiting lung inflammation and fibrosis. However, the precise mechanisms on lung cells themselves remain poorly understood. Here we investigated whether hMSC conditioned medium (hMSC-CM) would protect AECs from hypoxia-induced apoptosis and the mechanisms involved in this cytoprotective effect...
November 22, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29167124/microrna-1-is-decreased-by-hypoxia-and-contributes-to-the-development-of-pulmonary-vascular-remodeling-via-regulation-of-sphingosine-kinase-1
#8
Justin R Sysol, Jiwang Chen, Sunit Singla, Shuangping Zhao, Suzy A A Comhair, Viswanathan Natarajan, Roberto F Machado
Sphingosine Kinase 1 (SphK1) upregulation is associated with pathologic pulmonary vascular remodeling in pulmonary arterial hypertension (PAH), but the mechanisms controlling its expression are undefined. In this study, we sought to characterize the regulation of SphK1 expression by microRNAs (miRs). In silico analysis of the SphK1-3'UTR identified several putative miR binding sites, with miR-1-3p (miR-1) being the most highly predicted target. Therefore, we further investigated the role of miR-1 in modulating SPhK1 expression and characterized its effects on the phenotype of pulmonary artery smooth muscle cells (PASMCs) and the development of experimental pulmonary hypertension in vivo...
November 22, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29146576/accepting-the-challenge-maintaining-ajp-lung-as-the-best-place-to-publish-basic-and-translational-studies-in-lung-biology-and-pathophysiology
#9
Rory E Morty
Rory E. Morty takes over from Sadis Matalon as Editor-in-Chief of the American Journal of Physiology - Lung Cellular and Molecular Physiology in January 2018. Here, key achievements and new and noteworthy additions to the editorial portfolio of the Journal will be reviewed. Additionally, selected recent reports will be highlighted, and used to illustrate how the broad spectrum of the Journal's editorial content promotes methodological innovation and scientific advances in lung biology and pathophysiology.
November 16, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29146575/lumacaftor-vx-809-restores-the-ability-of-cf-macrophages-to-phagocytose-and-kill-pseudomonas-aeruginosa
#10
Roxanna Barnaby, Katja Koeppen, Amanda Nymon, Thomas H Hampton, Brent Berwin, Alix Ashare, Bruce Stanton
Cystic Fibrosis (CF), the most common lethal genetic disease in Caucasians, is characterized by chronic bacterial lung infection and excessive inflammation, which leads to progressive loss of lung function, and premature death. Although ivacaftor (VX-770) and the combination of ivacaftor and lumacaftor (VX-809) improve lung function in CF patients with the Gly551Asp and del508Phe mutation, respectively, the effects of these drugs on the function of human CF macrophages are unknown. Thus, studies were conducted to examine the effects of lumacaftor alone and in combination with ivacaftor (i...
November 16, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29146574/mast-cell-dependent-il-33-st2-signaling-is-protective-against-the-development-of-airway-hyperresponsiveness-in-a-house-dust-mite-mouse-model-of-asthma
#11
Anna Maria Zoltowska Nilsson, Ying Lei, Mikael Adner, Gunnar P Nilsson
Interleukin-33 (IL-33) and its receptor ST2 have been influentially associated to the pathophysiology of asthma. Due to the divergent roles of IL-33 in regulating mast cell functions, there is a need to further characterize IL-33/ST2-dependent mast cell responses and their significance in the context of asthma. This study aimed to investigate how IL-33/ST2-dependent mast cell responses contribute to the development of airway hyperresponsiveness (AHR) and airway inflammation in a mouse model of house dust mite (HDM) induced asthma...
November 16, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29146573/prostanoid-ep4-agonist-l-902-688-activates-ppar%C3%AE-and-attenuates-pulmonary-arterial-hypertension
#12
Hsin-Hsien Li, Hsao-Hsun Hsu, Gwo-Jyh Chang, I-Chen Chen, Wan-Jing Ho, Pei-Chen Hsu, Wei-Jan Chen, Jong-Hwei Su Pang, Chung-Chi Huang, Ying-Ju Lai
Prostacyclin agonists that bind the prostacyclin receptor (IP) to stimulate cyclic adenosine monophosphate (cAMP) synthesis are effective vasodilators for the treatment of idiopathic pulmonary arterial hypertension (IPAH) but this signaling may occur through nuclear peroxisome proliferator-activated receptor-gamma (PPARγ). There is evidence of scant IP and PPARγ expression but stable prostanoid EP4 receptor (EP4) expression in IPAH patients. Both IP and EP4 functionally couple with stimulatory G protein (Gs), which activate signal transduction...
November 16, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29122755/renin-angiotensin-system-regulates-pulmonary-arterial-smooth-muscle-cell-migration-in-chronic-thromboembolic-pulmonary-hypertension
#13
Yun Xia Zhang, Ji Feng Li, Yuan Hua Yang, Zhen Guo Zhai, Song Gu, Yan Liu, Ran Miao, Ping Ping Zhong, Ying Wang, Xiao Xi Huang, Chen Wang
Pulmonary arterial smooth muscle cell (PASMC) migration plays a key role in vascular remodeling which occurs during development of chronic thromboembolic pulmonary hypertension (CTEPH). Activation of the renin-angiotensin system (RAS) contributes to vascular remodeling observed in many diseases including idiopathic pulmonary arterial hypertension. However, the role of RAS imbalance in CTEPH has not been characterized. Here, we hypothesize that RAS imbalance regulates vascular remodeling by promoting PASMC migration in CTEPH...
November 9, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29122754/limited-role-of-kininogen-in-the-host-response-during-gram-negative-pneumonia-derived-sepsis
#14
Chao Ding, Cornelis Van't Veer, Joris J T H Roelofs, Meenal Shukla, Keith R McCrae, Alexey S Revenko, Jeff Crosby, Tom van der Poll
High molecular weight kininogen (HK), together with Factor XI, Factor XII and prekallikrein, is part of the contact system, which has proinflammatory, prothrombotic and vasoactive properties. We hypothesized that HK plays a role in the host response during pneumonia derived sepsis. To this end mice were depleted of kininogen (KNG) to plasma HK levels of 28% of normal by repeated treatment with a specific antisense oligonucleotide (KNG ASO) for three weeks prior to infection with the common human sepsis pathogen Klebsiella pneumoniae via the airways...
November 9, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29097427/nlrp3-inflammasome-activation-in-aged-macrophages-is-diminished-during-streptococcus-pneumoniae-infection
#15
Soo Jung Cho, Kristen T Rooney, Augustine M K Choi, Heather W Stout-Delgado
Pneumococcal infections are the 8th leading cause of death in the United States and it is estimated that older patients (>65 years of age) account for the most serious cases. The goal of our current study is to understand the impact of biological aging on innate immune responses to Streptococcus pneumoniae, a causative agent of bacterial pneumonia. Using in vitro and in vivo aged murine models, our findings demonstrate that age-enhanced unfolded protein responses (UPR) contribute to diminished inflammasome assembly and activation during S...
November 2, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29097426/the-emerging-role-of-angiogenesis-in-adaptive-and-maladaptive-right-ventricular-remodeling-in-pulmonary-hypertension
#16
Andrea L Frump, Sebastien Bonnet, Vinicio A de Jesus Perez, Tim Lahm
Right ventricular (RV) function is the primary prognostic factor for both morbidity and mortality in pulmonary hypertension (PH). RV hypertrophy is initially an adaptive physiological response to increased overload; however, with persistent and/or progressive afterload increase, this response frequently transitions to more pathological maladaptive remodeling. The mechanisms and disease processes underlying this transition are mostly unknown. Angiogenesis has recently emerged as a major modifier of RV adaptation in the setting of pressure overload...
November 2, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29097425/docosahexaenoic-acid-enhances-amphiregulin-mediated-bronchial-epithelial-cell-repair-processes-following-organic-dust-exposure
#17
Tara M Nordgren, Art J Heires, Kristina L Bailey, Dawn M Katafiasz, Myron L Toews, Christopher S Wichman, Debra J Romberger
Injurious dust exposures in the agricultural workplace involve the release of inflammatory mediators and activation of epidermal growth factor receptor (EGFR) in the respiratory epithelium. Amphiregulin, an EGFR ligand, mediates tissue repair and wound healing in the lung epithelium. Omega-3 fatty acids such as docosahexaenoic acid (DHA) are also known modulators of repair and resolution of inflammatory injury. This study investigated how AREG, DHA and EGFR modulate lung repair processes following dust-induced injury...
November 2, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29097424/the-free-fatty-acid-receptor-1-promotes-airway-smooth-muscle-cell-proliferation-through-mek-erk-and-pi3k-akt-signaling-pathways
#18
Atsuko Matoba, Nao Matsuyama, Sumire Shibata, Eiji Masaki, Charles W Emala, Kentaro Mizuta
Obesity is a risk factor for asthma and influences airway hyperresponsiveness, which is in part modulated by airway smooth muscle proliferative remodeling. Plasma free fatty acids (FFAs) levels are elevated in obese individuals, and long-chain FFAs act as endogenous ligands for the free fatty acid receptor 1 (FFAR1), which couples to both Gq and Gi proteins. We examined whether stimulation of FFAR1 induces airway smooth muscle cell proliferation through classical MEK/ERK and/or PI3K/Akt signaling pathways. The long-chain FFAs (oleic acid and linoleic acid) and a FFAR1 agonist (GW9508) induced human airway smooth muscle (HASM) cell proliferation, which was inhibited by the MEK inhibitor U0126 and the PI3K inhibitor LY294002...
November 2, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29097423/docosahexaenoic-acid-inhibits-monocrotaline-induced-pulmonary-hypertension-via-attenuating-endoplasmic-reticulum-stress-and-inflammation
#19
Rui Chen, Wei Zhong, Chen Shao, Peijing Liu, Cuiping Wang, Zhongqun Wang, Meiping Jiang, Yi Lu, Jinchuan Yan
Endoplasmic reticulum (ER) stress and inflammation contribute to pulmonary hypertension (PH) pathogenesis. Previously, we confirmed docosahexaenoic acid (DHA) could improve hypoxic-induced PH. However, little is known about the link between DHA and monocrotaline (MCT)-induced PH. Our aims were, therefore, to evaluate the effects and molecular mechanisms of DHA on MCT-induced PH in rat. Rat PH was induced by MCT. Rats were treated with DHA daily in prevention group (following MCT injection) and reversal group (after MCT injection for 2 weeks) by gavage...
November 2, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29074492/autophagy-inhibitor-3-methyladenine-protects-against-endothelial-cell-barrier-dysfunction-in-acute-lung-injury
#20
Spencer A Slavin, Antony Leonard, Valerie Grose, Fabeha Fazal, Arshad Rahman
Autophagy is an evolutionarily conserved cellular process that facilitates the continuous recycling of intracellular components (organelles and proteins) and provides an alternative source of energy when nutrients are scarce. Recent studies have implicated autophagy in many disorders including pulmonary diseases. However, the role of autophagy in endothelial cell (EC) barrier dysfunction and its relevance in the context of acute lung injury (ALI) remains uncertain. Here, we provide evidence that autophagy is a critical component of EC barrier disruption in ALI...
October 26, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
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