AJP: Lung Cellular and Molecular Physiology This is an RSS file. You can use it to subscribe to this data in your favourite RSS reader or to display this data on your own website or blog.

Inflammation and lung injury in an ovine model of extracorporeal membrane oxygenation support
Extracorporeal membrane oxygenation (ECMO) is a life-saving treatment for patients with severe refractory cardiorespiratory failure. Exposure to the ECMO circuit is thought to trigger/exacerbate inflammation. Determining whether inflammation is the result of the patients' underlying pathologies or the ECMO circuit is difficult. To discern how different insults contribute to the inflammatory response, we developed an ovine model of lung injury and ECMO to investigate the impact of smoke-induced lung injury and ECMO in isolation and cumulatively on pulmonary and circulating inflammatory cells, cytokines, and tissue remodelin...
Source: AJP: Lung Cellular and Molecular Physiology - December 11, 2016 Category: Respiratory Medicine Authors: Passmore, M. R., Fung, Y. L., Simonova, G., Foley, S. R., Dunster, K. R., Diab, S. D., Tung, J.-P., Minchinton, R. M., McDonald, C. I., Anstey, C. M., Shekar, K., Fraser, J. F. Tags: CALL FOR PAPERS Source Type: research

BRD4 mediates NF-{kappa}B-dependent epithelial-mesenchymal transition and pulmonary fibrosis via transcriptional elongation
Chronic epithelial injury triggers a TGF-β-mediated cellular transition from normal epithelium into a mesenchymal-like state that produces subepithelial fibrosis and airway remodeling. Here we examined how TGF-β induces the mesenchymal cell state and determined its mechanism. We observed that TGF-β stimulation activates an inflammatory gene program controlled by the NF-B/RelA signaling pathway. In the mesenchymal state, NF-B-dependent immediate-early genes accumulate euchromatin marks and processive RNA polymerase. This program of immediate-early genes is activated by enhanced expression, nuclear translocati...
Source: AJP: Lung Cellular and Molecular Physiology - December 11, 2016 Category: Respiratory Medicine Authors: Tian, B., Zhao, Y., Sun, H., Zhang, Y., Yang, J., Brasier, A. R. Tags: CALL FOR PAPERS Source Type: research

A sequence upstream of canonical PDZ-binding motif within CFTR COOH-terminus enhances NHERF1 interaction
In this study, we explored whether COOH-terminal sequences in CFTR beyond the PDZ-binding motif influence its interaction with NHERF1. NHERF1 displayed minimal self-association in blot overlays (NHERF1, Kd = 1,382 ± 61.1 nM) at concentrations well above physiological levels, estimated at 240 nM from RNA-sequencing and 260 nM by liquid chromatography tandem mass spectrometry in sweat gland, a key site of CFTR function in vivo. However, NHERF1 oligomerized at considerably lower concentrations (10 nM) in the presence of the last 111 amino acids of CFTR (20 nM) in blot overlays and cross-linking assays and in coimmunopr...
Source: AJP: Lung Cellular and Molecular Physiology - December 11, 2016 Category: Respiratory Medicine Authors: Sharma, N., LaRusch, J., Sosnay, P. R., Gottschalk, L. B., Lopez, A. P., Pellicore, M. J., Evans, T., Davis, E., Atalar, M., Na, C.-H., Rosson, G. D., Belchis, D., Milewski, M., Pandey, A., Cutting, G. R. Tags: CALL FOR PAPERS Source Type: research

Lethal H1N1 influenza A virus infection alters the murine alveolar type II cell surfactant lipidome
Alveolar type II (ATII) epithelial cells are the primary site of influenza virus replication in the distal lung. Development of acute respiratory distress syndrome in influenza-infected mice correlates with significant alterations in ATII cell function. However, the impact of infection on ATII cell surfactant lipid metabolism has not been explored. C57BL/6 mice were inoculated intranasally with influenza A/WSN/33 (H1N1) virus (10,000 plaque-forming units/mouse) or mock-infected with virus diluent. ATII cells were isolated by a standard lung digestion protocol at 2 and 6 days postinfection. Levels of 77 surfactant lipid-rel...
Source: AJP: Lung Cellular and Molecular Physiology - December 11, 2016 Category: Respiratory Medicine Authors: Woods, P. S., Doolittle, L. M., Rosas, L. E., Joseph, L. M., Calomeni, E. P., Davis, I. C. Tags: CALL FOR PAPERS Source Type: research

Epithelial disruption of Gab1 perturbs surfactant homeostasis and predisposes mice to lung injuries
In this study, in vitro knockdown of Gab1 was shown to decrease the surfactant proteins (SPs) levels in AT-IIs. We further examined in vivo Gab1 functions through alveolar epithelium-specific Gab1 knockout mice (Gab1/). In vivo Gab1 deficiency leads to a decrease in SP synthesis and the appearance of disorganized lamellar bodies. Histological analysis of the lung sections in Gab1/ mice shows no apparent pathological alterations or inflammation. However, Gab1/ mice demonstrate inflammatory responses during the LPS-induced acute lung injury. Similarly, in mice challenged with bleomycin, fibrotic lesions were found to be aggr...
Source: AJP: Lung Cellular and Molecular Physiology - December 11, 2016 Category: Respiratory Medicine Authors: Wang, K., Qin, S., Liang, Z., Zhang, Y., Xu, Y., Chen, A., Guo, X., Cheng, H., Zhang, X., Ke, Y. Tags: CALL FOR PAPERS Source Type: research

Chronic allergic pulmonary inflammation is aggravated in angiotensin-(1-7) Mas receptor knockout mice
The angiotensin-(1–7) [ANG-(1–7)]/Mas receptor pathway is currently recognized as a counterbalancing mechanism of the renin-angiotensin system in different pathophysiological conditions. We have previously described that treatment with ANG-(1–7) attenuates lung inflammation and remodeling in an experimental model of asthma. In the present study, we investigated whether lack of the Mas receptor could alter the inflammatory response in a model of chronic allergic lung inflammation induced by ovalbumin (OVA). Mas receptor wild-type (MasWT) and knockout (MasKO) mice were subjected to four doses of OVA (20 &mu...
Source: AJP: Lung Cellular and Molecular Physiology - December 11, 2016 Category: Respiratory Medicine Authors: Magalhaes, G. S., Rodrigues-Machado, M. G., Motta-Santos, D., Alenina, N., Bader, M., Santos, R. A., Barcelos, L. S., Campagnole-Santos, M. J. Tags: CALL FOR PAPERS Source Type: research

Emerging concepts in smooth muscle contributions to airway structure and function: implications for health and disease
Airway structure and function are key aspects of normal lung development, growth, and aging, as well as of lung responses to the environment and the pathophysiology of important diseases such as asthma, chronic obstructive pulmonary disease, and fibrosis. In this regard, the contributions of airway smooth muscle (ASM) are both functional, in the context of airway contractility and relaxation, as well as synthetic, involving production and modulation of extracellular components, modulation of the local immune environment, cellular contribution to airway structure, and, finally, interactions with other airway cell types such...
Source: AJP: Lung Cellular and Molecular Physiology - December 11, 2016 Category: Respiratory Medicine Authors: Prakash, Y. S. Tags: REVIEW Source Type: research

Interferon-{gamma} promotes double-stranded RNA-induced TLR3-dependent apoptosis via upregulation of transcription factor Runx3 in airway epithelial cells
Viral respiratory tract infections are the most common illness in humans. Infection of the respiratory viruses results in accumulation of viral replicative double-stranded RNA (dsRNA), which is one of the important components of infecting viruses for the induction of lung epithelial cell apoptosis and innate immune response, including the production of interferon (IFN). In the present study, we have investigated the regulation of dsRNA-induced airway epithelial cell apoptosis by IFN. We found that transcription factor Runx3 was strongly induced by type-II IFN, slightly by type-III IFN, but essentially not by type-I IFN&alp...
Source: AJP: Lung Cellular and Molecular Physiology - November 30, 2016 Category: Respiratory Medicine Authors: Gan, H., Hao, Q., Idell, S., Tang, H. Tags: ARTICLES Source Type: research

Endothelin-1-Rho kinase interactions impair lung structure and cause pulmonary hypertension after bleomycin exposure in neonatal rat pups
Bronchopulmonary dysplasia (BPD) is the chronic lung disease associated with premature birth, characterized by impaired vascular and alveolar growth. In neonatal rats bleomycin decreases lung growth and causes pulmonary hypertension (PH), which is poorly responsive to nitric oxide. In the developing lung, through Rho kinase (ROCK) activation, ET-1 impairs endothelial cell function; however, whether ET-1–ROCK interactions contribute to impaired vascular and alveolar growth in experimental BPD is unknown. Neonatal rats were treated daily with intraperitoneal bleomycin with and without selective ETA (BQ123/BQ610) and ET...
Source: AJP: Lung Cellular and Molecular Physiology - November 30, 2016 Category: Respiratory Medicine Authors: Gien, J., Tseng, N., Seedorf, G., Kuhn, K., Abman, S. H. Tags: ARTICLES Source Type: research

The total number of acini remains constant throughout postnatal rat lung development
The pulmonary airways are subdivided into conducting and gas-exchanging airways. The small tree of gas-exchanging airways which is fed by the most distal conducting airway represents an acinus. Very little is known about the development of the number of acini. The goal of this study was to estimate their number throughout rat postnatal development. Right middle rat lung lobes were obtained at postnatal day 4–60, stained with heavy metals, paraffin embedded, and scanned by synchrotron radiation-based X-ray tomographic microscopy or imaged with micro computed tomography after critical point drying. The acini were count...
Source: AJP: Lung Cellular and Molecular Physiology - November 30, 2016 Category: Respiratory Medicine Authors: Barre, S. F., Haberthür, D., Cremona, T. P., Stampanoni, M., Schittny, J. C. Tags: CALL FOR PAPERS Source Type: research

BNP, troponin I, and YKL-40 as screening markers in extremely preterm infants at risk for pulmonary hypertension associated with bronchopulmonary dysplasia
In conclusion, increased serum levels of BNP were associated with evidence of TR at 36-wk corrected gestational age in extremely preterm infants, suggesting a potential role as a screening biomarker for BPD-associated PH. (Source: AJP: Lung Cellular and Molecular Physiology)
Source: AJP: Lung Cellular and Molecular Physiology - November 30, 2016 Category: Respiratory Medicine Authors: König, K., Guy, K. J., Nold-Petry, C. A., Barfield, C. P., Walsh, G., Drew, S. M., Veldman, A., Nold, M. F., Casalaz, D. M. Tags: CALL FOR PAPERS Source Type: research

Neutrophils promote alveolar epithelial regeneration by enhancing type II pneumocyte proliferation in a model of acid-induced acute lung injury
Alveolar epithelial regeneration is essential for resolution of the acute respiratory distress syndrome (ARDS). Although neutrophils have traditionally been considered mediators of epithelial damage, recent studies suggest they promote type II pneumocyte (AT2) proliferation, which is essential for regenerating alveolar epithelium. These studies did not, however, evaluate this relationship in an in vivo model of alveolar epithelial repair following injury. To determine whether neutrophils influence alveolar epithelial repair in vivo, we developed a unilateral acid injury model that creates a severe yet survivable injury wit...
Source: AJP: Lung Cellular and Molecular Physiology - November 30, 2016 Category: Respiratory Medicine Authors: Paris, A. J., Liu, Y., Mei, J., Dai, N., Guo, L., Spruce, L. A., Hudock, K. M., Brenner, J. S., Zacharias, W. J., Mei, H. D., Slamowitz, A. R., Bhamidipati, K., Beers, M. F., Seeholzer, S. H., Morrisey, E. E., Worthen, G. S. Tags: ARTICLES Source Type: research

MicroRNA-29c regulates apoptosis sensitivity via modulation of the cell-surface death receptor, Fas, in lung fibroblasts
MicroRNAs play an important role in the development and progression of various diseases, such as idiopathic pulmonary fibrosis (IPF). Although the accumulation of aberrant fibroblasts resistant to apoptosis is a hallmark in IPF lungs, the mechanism regulating apoptosis susceptibility is not fully understood. Here, we investigated the role of miR-29, which is the most downregulated microRNA in IPF lungs and is also known as a regulator of extracellular matrix (ECM), in the mechanism of apoptosis resistance. We found that functional inhibition of miR-29c caused resistance to Fas-mediated apoptosis in lung fibroblasts. Furthe...
Source: AJP: Lung Cellular and Molecular Physiology - November 30, 2016 Category: Respiratory Medicine Authors: Matsushima, S., Ishiyama, J. Tags: ARTICLES Source Type: research

Rac1 modulates mammalian lung branching morphogenesis in part through canonical Wnt signaling
Lung branching morphogenesis relies on a number of factors, including proper epithelial cell proliferation and differentiation, cell polarity, and migration. Rac1, a small Rho GTPase, orchestrates a number of these cellular processes, including cell proliferation and differentiation, cellular alignment, and polarization. Furthermore, Rac1 modulates both noncanonical and canonical Wnt signaling, important pathways in lung branching morphogenesis. Culture of embryonic mouse lung explants in the presence of the Rac1 inhibitor (NSC23766) resulted in a dose-dependent decrease in branching. Increased cell death and BrdU uptake w...
Source: AJP: Lung Cellular and Molecular Physiology - November 30, 2016 Category: Respiratory Medicine Authors: Danopoulos, S., Krainock, M., Toubat, O., Thornton, M., Grubbs, B., Al Alam, D. Tags: CALL FOR PAPERS Source Type: research

Nur77 attenuates endothelin-1 expression via downregulation of NF-{kappa}B and p38 MAPK in A549 cells and in an ARDS rat model
The objective of this study is to investigate the potential role of Nur77 and its underlying mechanism in the regulation of endothelin-1 (ET-1) expression in lipopolysaccharide (LPS)-induced A549 cells and an ARDS rat model. We demonstrate that LPS induced Nur77 expression and nuclear export in A549 cells. Overexpression of Nur77 markedly decreased basal and LPS-induced ET-1 expression in A549 cells, whereas knockdown of Nur77 increased the ET-1 expression. LPS-induced phosphorylation and nuclear translocation of NF-B and p38 MAPK were blocked by Nur77 overexpression and augmented by Nur77 knockdown in A549 cells. In vivo,...
Source: AJP: Lung Cellular and Molecular Physiology - November 30, 2016 Category: Respiratory Medicine Authors: Jiang, Y., Zeng, Y., Huang, X., Qin, Y., Luo, W., Xiang, S., Sooranna, S. R., Pinhu, L. Tags: CALL FOR PAPERS Source Type: research