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.

A new target for caffeine in the developing lung: endoplasmic reticulum stress?
(Source: AJP: Lung Cellular and Molecular Physiology)
Source: AJP: Lung Cellular and Molecular Physiology - October 1, 2017 Category: Respiratory Medicine Authors: Rath, P., Nardiello, C., Morty, R. E. Tags: EDITORIAL FOCUS Source Type: research

The beginnings of cardiac catheterization and the resulting impact on pulmonary medicine
The early history of cardiac catheterization has many interesting features. First, although it would be natural to assume that the procedure was initiated by cardiologists, two of the three people who shared the Nobel Prize for the discovery were pulmonologists, while the third was a urologist. The primary objective of the pulmonologists André Cournand and Dickinson Richards was to obtain mixed venous blood from the right heart so that they could use the Fick principle to calculate total pulmonary blood flow. Cournand’s initial catheterization studies were prompted by his reading of an account by Werner Forssm...
Source: AJP: Lung Cellular and Molecular Physiology - October 1, 2017 Category: Respiratory Medicine Authors: West, J. B. Tags: REVIEW Source Type: research

Letter to the editor: BET inhibitors might target innate inflammatory and profibrotic signaling networks in COPD
(Source: AJP: Lung Cellular and Molecular Physiology)
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2017 Category: Respiratory Medicine Authors: Du, J., Han, Y. Tags: LETTER TO THE EDITOR Source Type: research

Arterial stiffness induces remodeling phenotypes in pulmonary artery smooth muscle cells via YAP/TAZ-mediated repression of cyclooxygenase-2
Pulmonary arterial stiffness is an independent risk factor for mortality in pulmonary hypertension (PH) and plays a critical role in PH pathophysiology. Our laboratory has recently demonstrated arterial stiffening early in experimental PH, along with evidence for a mechanobiological feedback loop by which arterial stiffening promotes further cellular remodeling behaviors (Liu F, Haeger CM, Dieffenbach PB, Sicard D, Chrobak I, Coronata AM, Suárez Velandia MM, Vitali S, Colas RA, Norris PC, Marinković A, Liu X, Ma J, Rose CD, Lee SJ, Comhair SA, Erzurum SC, McDonald JD, Serhan CN, Walsh SR, Tschumperlin DJ, Fre...
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2017 Category: Respiratory Medicine Authors: Dieffenbach, P. B., Haeger, C. M., Coronata, A. M. F., Choi, K. M., Varelas, X., Tschumperlin, D. J., Fredenburgh, L. E. Tags: RESEARCH ARTICLE Source Type: research

Transforming growth factor-{beta} stimulates Smad1/5 signaling in pulmonary artery smooth muscle cells and fibroblasts of the newborn mouse through ALK1
The intracellular signaling mechanisms through which TGF-β regulates pulmonary development are incompletely understood. Canonical TGF-β signaling involves Smad2/3 phosphorylation, Smad2/3·Smad4 complex formation and nuclear localization, and gene regulation. Here, we show that physiologically relevant TGF-β1 levels also stimulate Smad1/5 phosphorylation, which is 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. This cross-talk mechanism likely has in vivo relevance...
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2017 Category: Respiratory Medicine Authors: Zhang, H., Du, L., Zhong, Y., Flanders, K. C., Roberts, J. D. Tags: RESEARCH ARTICLE Source Type: research

The metalloproteinase ADAM8 promotes leukocyte recruitment in vitro and in acute lung inflammation
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. Furthermore, ADAM8 promotes αL-integrin upregulation and THP-1 cell adhesion to...
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2017 Category: Respiratory Medicine Authors: Dreymueller, D., Pruessmeyer, J., Schumacher, J., Fellendorf, S., Hess, F. M., Seifert, A., Babendreyer, A., Bartsch, J. W., Ludwig, A. Tags: RESEARCH ARTICLE Source Type: research

Impaired TNF/TNFR2 signaling enhances Th2 and Th17 polarization and aggravates allergic airway inflammation
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. The mouse model was generated by immunization with ovalbumin 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-...
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2017 Category: Respiratory Medicine Authors: Li, X.-M., Chen, X., Gu, W., Guo, Y.-J., Cheng, Y., Peng, J., Guo, X.-J. Tags: RESEARCH ARTICLE Source Type: research

Cigarette smoke disrupts monolayer integrity by altering epithelial cell-cell adhesion and cortical tension
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. Normal human airway epithelial cells and primary COPD epithelial cells were exposed to air or CS, and changes meas...
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2017 Category: Respiratory Medicine Authors: Nishida, K., Brune, K. A., Putcha, N., Mandke, P., ONeal, W. K., Shade, D., Srivastava, V., Wang, M., Lam, H., An, S. S., Drummond, M. B., Hansel, N. N., Robinson, D. N., Sidhaye, V. K. Tags: RESEARCH ARTICLE Source Type: research

Genetic variance is associated with susceptibility for cigarette smoke-induced DAMP release in mice
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. We tested whether small interfering RNA-dependent knockdown of candidate genes altered the susceptibility o...
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2017 Category: Respiratory Medicine Authors: Pouwels, S. D., Faiz, A., den Boef, L. E., Gras, R., van den Berge, M., Boezen, H. M., Korstanje, R., ten Hacken, N. H. T., van Oosterhout, A. J. M., Heijink, I. H., Nawijn, M. C. Tags: RESEARCH ARTICLE Source Type: research

Myeloid-epithelial cross talk coordinates synthesis of the tissue-protective cytokine leukemia inhibitory factor during pneumonia
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 acute respiratory distress syndrome. 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...
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2017 Category: Respiratory Medicine Authors: Traber, K. E., Symer, E. M., Allen, E., Kim, Y., Hilliard, K. L., Wasserman, G. A., Stewart, C. L., Jones, M. R., Mizgerd, J. P., Quinton, L. J. Tags: RESEARCH ARTICLE Source Type: research

Elastin receptor (S-gal) occupancy by elastin peptides modulates T-cell response during murine emphysema
This study demonstrates that, during murine emphysema, EP-S-gal interactions contribute to a Th-1 and Th-17 proinflammatory T-cell response combined with a Tc-1 response. Our study also highlights the S-gal receptor as a putative pharmacological target to modulate such an immune response. (Source: AJP: Lung Cellular and Molecular Physiology)
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2017 Category: Respiratory Medicine Authors: Meghraoui-Kheddar, A., Pierre, A., Sellami, M., Audonnet, S., Lemaire, F., Le Naour, R. Tags: RESEARCH ARTICLE Source Type: research

Impact of ventilation-induced lung injury on the structure and function of lamellar bodies
Alterations to the pulmonary surfactant system have been observed consistently in ventilation-induced lung injury (VILI) 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 body numbers and function. To test this hypothesis, rats were randomized to one of three groups, nonventilated controls, control ventilation, and high tidal volume ventilation (VILI). Following p...
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2017 Category: Respiratory Medicine Authors: Milos, S., Khazaee, R., McCaig, L. A., Nygard, K., Gardiner, R. B., Zuo, Y. Y., Yamashita, C., Veldhuizen, R. Tags: RESEARCH ARTICLE Source Type: research

Long-term nicotine exposure dampens LPS-induced nerve-mediated airway hyperreactivity in murine airways
In conclusion, long-term nicotine exposure dampened LPS-induced AHR. The effect of nicotine was mimicked by TTX, suggesting the involvement of neuronal mechanisms. This information might be used for evaluating the long-term effects of nicotine and further exploring of how tobacco products interact with bacterial airway infections. (Source: AJP: Lung Cellular and Molecular Physiology)
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2017 Category: Respiratory Medicine Authors: Xu, Y., Cardell, L.-O. Tags: RESEARCH ARTICLE Source Type: research

The PDE4 inhibitor CHF-6001 and LAMAs inhibit bronchoconstriction-induced remodeling in lung slices
Combination therapy of PDE4 inhibitors and anticholinergics induces bronchoprotection in COPD. Mechanical forces that arise during bronchoconstriction may contribute to airway remodeling. Therefore, we investigated the impact of PDE4 inhibitors and anticholinergics on bronchoconstriction-induced remodeling. Because of the different mechanism of action of PDE4 inhibitors and anticholinergics, we hypothesized functional interactions of these two drug classes. Guinea pig precision-cut lung slices were preincubated with the PDE4 inhibitors CHF-6001 or roflumilast and/or the anticholinergics tiotropium or glycopyorrolate, follo...
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2017 Category: Respiratory Medicine Authors: Kistemaker, L. E. M., Oenema, T. A., Baarsma, H. A., Bos, I. S. T., Schmidt, M., Facchinetti, F., Civelli, M., Villetti, G., Gosens, R. Tags: RESEARCH ARTICLE Source Type: research

Novel role of NPY in neuroimmune interaction and lung growth after intrauterine growth restriction
Individuals with intrauterine growth restriction (IUGR) are at risk for chronic lung disease. Using a rat model, we showed in our previous studies that altered lung structure is related to IL-6/STAT3 signaling. As neuropeptide Y (NPY), a coneurotransmitter of the sympathetic nervous 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. Finally, primary neonatal lung myo...
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2017 Category: Respiratory Medicine Authors: Thangaratnarajah, C., Dinger, K., Vohlen, C., Klaudt, C., Nawabi, J., Lopez Garcia, E., Kwapiszewska, G., Dobner, J., Nüsken, K. D., van Koningsbruggen-Rietschel, S., von Hörsten, S., Dötsch, J., Alejandre Alcazar, M. A. Tags: RESEARCH ARTICLE Source Type: research