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Source: AJP: Lung Cellular and Molecular Physiology
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Total 59 results found since Jan 2013.
Lipopolysaccharide induces ICAM-1 expression via a c-Src/NADPH oxidase/ROS-dependent NF-{kappa}B pathway in human pulmonary alveolar epithelial cells
Upregulation of intercellular adhesion molecule-1 (ICAM-1) is frequently implicated in lung inflammation. Lipopolysaccharide (LPS) has been shown to play a key role in inflammation via adhesion molecule induction and then causes lung injury. However, the mechanisms underlying LPS-induced ICAM-1 expression in human pulmonary alveolar epithelial cells (HPAEpiCs) remain unclear. We showed that LPS induced ICAM-1 expression in HPAEpiCs, revealed by Western blotting, RT-PCR, real-time PCR, and promoter assay. Pretreatment with the inhibitor of c-Src (protein phosphatase-1, PP1), reactive oxygen species (ROS) (Edaravone), NADPH ...
Source: AJP: Lung Cellular and Molecular Physiology - March 31, 2016 Category: Respiratory Medicine Authors: Cho, R.-L., Yang, C.-C., Lee, I.-T., Lin, C.-C., Chi, P.-L., Hsiao, L.-D., Yang, C.-M. Tags: ARTICLES Source Type: research
Targeting host calpain proteases decreases influenza A virus infection
Influenza A viruses (IAV) trigger contagious acute respiratory diseases. A better understanding of the molecular mechanisms of IAV pathogenesis and host immune responses is required for the development of more efficient treatments of severe influenza. Calpains are intracellular proteases that participate in diverse cellular responses, including inflammation. Here, we used in vitro and in vivo approaches to investigate the role of calpain signaling in IAV pathogenesis. Calpain expression and activity were found altered in IAV-infected bronchial epithelial cells. With the use of small-interfering RNA (siRNA) gene silencing, ...
Source: AJP: Lung Cellular and Molecular Physiology - March 31, 2016 Category: Respiratory Medicine Authors: Blanc, F., Furio, L., Moisy, D., Yen, H.-L., Chignard, M., Letavernier, E., Naffakh, N., Mok, C. K. P., Si-Tahar, M. Tags: ARTICLES Source Type: research
Augmentation of CFTR maturation by S-nitrosoglutathione reductase
S-nitrosoglutathione (GSNO) reductase regulates novel endogenous S-nitrosothiol signaling pathways, and mice deficient in GSNO reductase are protected from airways hyperreactivity. S-nitrosothiols are present in the airway, and patients with cystic fibrosis (CF) tend to have low S-nitrosothiol levels that may be attributed to upregulation of GSNO reductase activity. The present study demonstrates that 1) GSNO reductase activity is increased in the cystic fibrosis bronchial epithelial (CFBE41o–) cells expressing mutant F508del-cystic fibrosis transmembrane regulator (CFTR) compared with the wild-type CFBE41o– ce...
Source: AJP: Lung Cellular and Molecular Physiology - February 1, 2016 Category: Respiratory Medicine Authors: Zaman, K., Sawczak, V., Zaidi, A., Butler, M., Bennett, D., Getsy, P., Zeinomar, M., Greenberg, Z., Forbes, M., Rehman, S., Jyothikumar, V., DeRonde, K., Sattar, A., Smith, L., Corey, D., Straub, A., Sun, F., Palmer, L., Periasamy, A., Randell, S., Kelley Tags: CALL FOR PAPERS Source Type: research
Raf/ERK drives the proliferative and invasive phenotype of BMPR2-silenced pulmonary artery endothelial cells
This study examined the noncanonical signaling consequences of BMPR2 silencing in human pulmonary artery endothelial cells to identify potential therapeutic targets. BMPR2 siRNA silencing resulted in a proliferative, promigratory pulmonary artery endothelial cell phenotype and disruption of cytoskeletal architecture. Expression profiling closely reflected these phenotypic changes. Gene set enrichment and promoter analyses, as well as the differential expression of pathway components identified Ras/Raf/ERK signaling as an important consequence of BMPR2 silencing. Raf family members and ERK1/2 were constitutively activated a...
Source: AJP: Lung Cellular and Molecular Physiology - January 15, 2016 Category: Respiratory Medicine Authors: Awad, K. S., Elinoff, J. M., Wang, S., Gairhe, S., Ferreyra, G. A., Cai, R., Sun, J., Solomon, M. A., Danner, R. L. Tags: ARTICLES Source Type: research
Hydrogen peroxide-induced calcium influx in lung microvascular endothelial cells involves TRPV4
In conclusion, our data suggest that application of exogenous H2O2 increases [Ca2+]i and decreases TER in microvascular endothelial cells via activation of TRPV4 through a mechanism that requires the Src kinase Fyn.
Source: AJP: Lung Cellular and Molecular Physiology - December 15, 2015 Category: Respiratory Medicine Authors: Suresh, K., Servinsky, L., Reyes, J., Baksh, S., Undem, C., Caterina, M., Pearse, D. B., Shimoda, L. A. Tags: CALL FOR PAPERS Source Type: research
Pharmacologic inhibition of lactate production prevents myofibroblast differentiation
Myofibroblasts are one of the primary cell types responsible for the accumulation of extracellular matrix in fibrosing diseases, and targeting myofibroblast differentiation is an important therapeutic strategy for the treatment of pulmonary fibrosis. Transforming growth factor-β (TGF-β) has been shown to be an important inducer of myofibroblast differentiation. We previously demonstrated that lactate dehydrogenase and its metabolic product lactic acid are important mediators of myofibroblast differentiation, via acid-induced activation of latent TGF-β. Here we explore whether pharmacologic inhibition of LDH ...
Source: AJP: Lung Cellular and Molecular Physiology - December 1, 2015 Category: Respiratory Medicine Authors: Kottmann, R. M., Trawick, E., Judge, J. L., Wahl, L. A., Epa, A. P., Owens, K. M., Thatcher, T. H., Phipps, R. P., Sime, P. J. Tags: CALL FOR PAPERS Source Type: research
Protocadherin-1 binds to SMAD3 and suppresses TGF-{beta}1-induced gene transcription
In conclusion, we demonstrate that PCDH1 binds to SMAD3 and regulates its activation by TGF-β signaling in bronchial epithelial cells. We propose that PCDH1 and SMAD3 act in a single pathway in asthma susceptibility that affects sensitivity of the airway epithelium to TGF-β.
Source: AJP: Lung Cellular and Molecular Physiology - October 1, 2015 Category: Respiratory Medicine Authors: Faura Tellez, G., Vandepoele, K., Brouwer, U., Koning, H., Elderman, R. M., Hackett, T.-L., Willemse, B. W. M., Holloway, J., Van Roy, F., Koppelman, G. H., Nawijn, M. C. Tags: ARTICLES Source Type: research
Neutral sphingomyelinase 2 is required for cytokine-induced skeletal muscle calpain activation
Calpain contributes to infection-induced diaphragm dysfunction but the upstream mechanism(s) responsible for calpain activation are poorly understood. It is known, however, that cytokines activate neutral sphingomyelinase (nSMase) and nSMase has downstream effects with the potential to increase calpain activity. We tested the hypothesis that infection-induced skeletal muscle calpain activation is a consequence of nSMase activation. We administered cytomix (20 ng/ml TNF-α, 50 U/ml IL-1β, 100 U/ml IFN-, 10 μg/ml LPS) to C2C12 muscle cells to simulate the effects of infection in vitro and studied mice undergoing...
Source: AJP: Lung Cellular and Molecular Physiology - September 15, 2015 Category: Respiratory Medicine Authors: Supinski, G. S., Alimov, A. P., Wang, L., Song, X.-H., Callahan, L. A. Tags: ARTICLES Source Type: research
IFN-{gamma}-induced JAK/STAT, but not NF-{kappa}B, signaling pathway is insensitive to glucocorticoid in airway epithelial cells
Although the majority of patients with asthma are well controlled by inhaled glucocorticoids (GCs), patients with severe asthma are poorly responsive to GCs. This latter group is responsible for a disproportionate share of health care costs associated with asthma. Recent studies in immune cells have incriminated interferon- (IFN-) as a possible trigger of GC insensitivity in severe asthma; however, little is known about the role of IFN- in modulating GC effects in other clinically relevant nonimmune cells, such as airway epithelial cells. We hypothesized that IFN--induced JAK/STAT-associated signaling pathways in airway ep...
Source: AJP: Lung Cellular and Molecular Physiology - August 15, 2015 Category: Respiratory Medicine Authors: O'Connell, D., Bouazza, B., Kokalari, B., Amrani, Y., Khatib, A., Ganther, J. D., Tliba, O. Tags: CALL FOR PAPERS Source Type: research
Endothelin-1 induces VCAM-1 expression-mediated inflammation via receptor tyrosine kinases and Elk/p300 in human tracheal smooth muscle cells
The elevated level of endothelin-1 (ET-1) has been detected in the bronchoalveolar lavage of patients with severe asthma, acute lung injury, acute respiratory distress syndrome, and sepsis. ET-1 may affect vessel tone together with lung physiology and pathology. Vascular cell adhesion molecule-1 (VCAM-1) is one kind of adhesion molecules participating in the process of polymorphonuclear leukocyte transmigration and regulating the occurrence and amplification of tissue inflammation. However, the molecular mechanisms underlying ET-1-mediated expression of VCAM-1 on human tracheal smooth muscle cells (HTSMCs) were largely unk...
Source: AJP: Lung Cellular and Molecular Physiology - August 1, 2015 Category: Respiratory Medicine Authors: Lin, C.-C., Lin, W.-N., Hou, W.-C., Hsiao, L.-D., Yang, C.-M. Tags: CALL FOR PAPERS Source Type: research
Human airway smooth muscle cells secrete amphiregulin via bradykinin/COX-2/PGE2, inducing COX-2, CXCL8, and VEGF expression in airway epithelial cells
Human airway smooth muscle cells (HASMC) contribute to asthma pathophysiology through an increased smooth muscle mass and elevated cytokine/chemokine output. Little is known about how HASMC and the airway epithelium interact to regulate chronic airway inflammation and remodeling. Amphiregulin is a member of the family of epidermal growth factor receptor (EGFR) agonists with cell growth and proinflammatory roles and increased expression in the lungs of asthma patients. Here we show that bradykinin (BK) stimulation of HASMC increases amphiregulin secretion in a mechanism dependent on BK-induced COX-2 expression, increased PG...
Source: AJP: Lung Cellular and Molecular Physiology - August 1, 2015 Category: Respiratory Medicine Authors: Deacon, K., Knox, A. J. Tags: CALL FOR PAPERS Source Type: research
Influence of glutathione-S-transferase (GST) inhibition on lung epithelial cell injury: role of oxidative stress and metabolism
Oxidant-mediated tissue injury is key to the pathogenesis of acute lung injury. Glutathione-S-transferases (GSTs) are important detoxifying enzymes that catalyze the conjugation of glutathione with toxic oxidant compounds and are associated with acute and chronic inflammatory lung diseases. We hypothesized that attenuation of cellular GST enzymes would augment intracellular oxidative and metabolic stress and induce lung cell injury. Treatment of murine lung epithelial cells with GST inhibitors, ethacrynic acid (EA), and caffeic acid compromised lung epithelial cell viability in a concentration-dependent manner. These inhib...
Source: AJP: Lung Cellular and Molecular Physiology - June 15, 2015 Category: Respiratory Medicine Authors: Fletcher, M. E., Boshier, P. R., Wakabayashi, K., Keun, H. C., Smolenski, R. T., Kirkham, P. A., Adcock, I. M., Barton, P. J., Takata, M., Marczin, N. Tags: ARTICLES Source Type: research
c-Abl mediated tyrosine phosphorylation of paxillin regulates LPS-induced endothelial dysfunction and lung injury
Paxillin is phosphorylated at multiple residues; however, the role of tyrosine phosphorylation of paxillin in endothelial barrier dysfunction and acute lung injury (ALI) remains unclear. We used siRNA and site-specific nonphosphorylable mutants of paxillin to abrogate the function of paxillin to determine its role in lung endothelial permeability and ALI. In vitro, lipopolysaccharide (LPS) challenge of human lung microvascular endothelial cells (HLMVECs) resulted in enhanced tyrosine phosphorylation of paxillin at Y31 and Y118 with no significant change in Y181 and significant barrier dysfunction. Knockdown of paxillin wit...
Source: AJP: Lung Cellular and Molecular Physiology - May 15, 2015 Category: Respiratory Medicine Authors: Fu, P., Usatyuk, P. V., Lele, A., Harijith, A., Gregorio, C. C., Garcia, J. G. N., Salgia, R., Natarajan, V. Tags: CALL FOR PAPERS Source Type: research
p53 protects against LPS-induced lung endothelial barrier dysfunction
New therapies toward heart and blood vessel disorders may emerge from the development of Hsp90 inhibitors. Several independent studies suggest potent anti-inflammatory activities of those agents in human tissues. The molecular mechanisms responsible for their protective effects in the vasculature remain unclear. The present study demonstrates that the transcription factor p53, an Hsp90 client protein, is crucial for the maintenance of vascular integrity, protects again LPS-induced endothelial barrier dysfunction, and is involved in the mediation of the anti-inflammatory activity of Hsp90 inhibitors in lung tissues. p53 sil...
Source: AJP: Lung Cellular and Molecular Physiology - April 15, 2015 Category: Respiratory Medicine Authors: Barabutis, N., Dimitropoulou, C., Birmpas, C., Joshi, A., Thangjam, G., Catravas, J. D. Tags: CALL FOR PAPERS Source Type: research
Silencing of MUC8 by siRNA increases P2Y2-induced airway inflammation
Mucin hypersecretion and overproduction are frequent manifestations of respiratory disease. Determining the physiological function of airway mucin is presently considered more important than identifying the relevant signaling pathways. The lack of a full-length human mucin 8 (MUC8) cDNA sequence has hindered the generation of a Muc8 knockout mouse line. Thus, the precise physiological functions of MUC8 are unclear. Herein, we investigated the function of MUC8 using a small-interfering RNA (siRNA)-mediated genetic silencing approach in human airway epithelial cells. Herein, intracellular IL-1α production was stimulate...
Source: AJP: Lung Cellular and Molecular Physiology - March 15, 2015 Category: Respiratory Medicine Authors: Cha, H.-J., Jung, M.-S., Ahn, D. W., Choi, J.-K., Ock, M. S., Kim, K. S., Yoon, J.-H., Song, E. J., Song, K. S. Tags: CALL FOR PAPERS Source Type: research
