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Source: AJP: Lung Cellular and Molecular Physiology
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Total 59 results found since Jan 2013.
Endothelin-1 decreases endothelial PPAR{gamma} signaling and impairs angiogenesis after chronic intrauterine pulmonary hypertension
Increased endothelin-1 (ET-1) disrupts angiogenesis in persistent pulmonary hypertension of the newborn (PPHN), but pathogenic mechanisms are unclear. Peroxisome proliferator activated receptor (PPAR) is decreased in adult pulmonary hypertension, but whether ET-1-PPAR interactions impair endothelial cell function and angiogenesis in PPHN remains unknown. We hypothesized that increased PPHN pulmonary artery endothelial cell (PAEC) ET-1 production decreases PPAR signaling and impairs tube formation in vitro. Proximal PAECs were harvested from fetal sheep after partial ligation of the ductus arteriosus in utero (PPHN) and con...
Source: AJP: Lung Cellular and Molecular Physiology - February 15, 2014 Category: Respiratory Medicine Authors: Wolf, D., Tseng, N., Seedorf, G., Roe, G., Abman, S. H., Gien, J. Tags: ARTICLES Source Type: research
Peroxisome proliferator activated receptor-{gamma}-Rho-kinase interactions contribute to vascular remodeling after chronic intrauterine pulmonary hypertension
Peroxisome proliferator-activated receptor- (PPAR) and Rho-kinase (ROCK) regulate smooth muscle cell (SMC) proliferation and contribute to vascular remodeling in adult pulmonary hypertension. Whether these pathways interact to contribute to the development of vascular remodeling in persistent pulmonary hypertension of the newborn (PPHN) remains unknown. We hypothesized that ROCK-PPAR interactions increase SMC proliferation resulting in vascular remodeling in experimental PPHN. Pulmonary artery SMCs (PASMCs) were harvested from fetal sheep after partial ligation of the ductus arteriosus in utero (PPHN) and controls. Cell co...
Source: AJP: Lung Cellular and Molecular Physiology - February 1, 2014 Category: Respiratory Medicine Authors: Gien, J., Tseng, N., Seedorf, G., Roe, G., Abman, S. H. Tags: ARTICLES Source Type: research
Autophagy mediates avian influenza H5N1 pseudotyped particle-induced lung inflammation through NF-{kappa}B and p38 MAPK signaling pathways
Since avian influenza virus H5N1-induced hypercytokemia plays a key role in acute lung injury, understanding its molecular mechanism is highly desirable for discovering therapeutic targets against H5N1 infection. In the present study, we investigated the role of autophagy in H5N1-induced lung inflammation by using H5N1 pseudotyped viral particles (H5N1pps). The results showed that H5N1pps significantly induced autophagy both in A549 human lung epithelial cells and in mouse lung tissues, which was primarily due to hemagglutinin (HA) of H5N1 virus. Blocking autophagy with 3-methyladenine (an autophagy inhibitor) or siRNA kno...
Source: AJP: Lung Cellular and Molecular Physiology - January 15, 2014 Category: Respiratory Medicine Authors: Pan, H., Zhang, Y., Luo, Z., Li, P., Liu, L., Wang, C., Wang, H., Li, H., Ma, Y. Tags: ARTICLES Source Type: research
Trop2 regulates motility and lamellipodia formation in cultured fetal lung fibroblasts
Proliferation and migration of fibroblasts are vital for fetal lung development. However, the regulatory mechanisms are poorly understood. We have previously shown that TROP2 gene expression is closely associated with fetal lung cell proliferation in vivo and that TROP2 knockdown decreases proliferation of fetal lung fibroblasts in culture. We hypothesized that the Trop2 protein also regulates the morphology and motility of fetal lung fibroblasts. Fibroblasts isolated from fetal rat lungs (gestational age embryonic day 19) adopted a myofibroblast-like morphology in culture. Trop2 protein was localized to lamellipodia. TROP...
Source: AJP: Lung Cellular and Molecular Physiology - October 1, 2013 Category: Respiratory Medicine Authors: McDougall, A. R. A., Hooper, S. B., Zahra, V. A., Cole, T. J., Lo, C. Y., Doran, T., Wallace, M. J. Tags: ARTICLES Source Type: research
Transdifferentiation of alveolar epithelial type II to type I cells is controlled by opposing TGF-{beta} and BMP signaling
Alveolar epithelial type II (ATII) cells are essential for maintaining normal lung homeostasis because they produce surfactant, express innate immune proteins, and can function as progenitors for alveolar epithelial type I (ATI) cells. Although autocrine production of transforming growth factor (TGF)-β1 has been shown to promote the transdifferentiation of primary rat ATII to ATI cells in vitro, mechanisms controlling this process still remain poorly defined. Here, evidence is provided that Tgf-β1, -2, -3 mRNA and phosphorylated SMAD2 and SMAD3 significantly increase as primary cultures of mouse ATII cells transd...
Source: AJP: Lung Cellular and Molecular Physiology - September 15, 2013 Category: Respiratory Medicine Authors: Zhao, L., Yee, M., O'Reilly, M. A. Tags: ARTICLES Source Type: research
Id proteins are critical downstream effectors of BMP signaling in human pulmonary arterial smooth muscle cells
In conclusion, Id proteins, and particularly Id1 and Id3, are critical downstream effectors of BMP signaling in PASMCs. Loss of BMPR-II function reduces the induction of Id genes in PASMCs, Id1, and Id3 regulate the proliferation of PASMCs via cell cycle inhibition, an effect that may be exacerbated by inflammatory stimuli.
Source: AJP: Lung Cellular and Molecular Physiology - August 15, 2013 Category: Respiratory Medicine Authors: Yang, J., Li, X., Li, Y., Southwood, M., Ye, L., Long, L., Al-Lamki, R. S., Morrell, N. W. Tags: ARTICLES Source Type: research
Ezrin/radixin/moesin proteins differentially regulate endothelial hyperpermeability after thrombin
Endothelial cell (EC) barrier disruption induced by inflammatory agonists such as thrombin leads to potentially lethal physiological dysfunction such as alveolar flooding, hypoxemia, and pulmonary edema. Thrombin stimulates paracellular gap and F-actin stress fiber formation, triggers actomyosin contraction, and alters EC permeability through multiple mechanisms that include protein kinase C (PKC) activation. We previously have shown that the ezrin, radixin, and moesin (ERM) actin-binding proteins differentially participate in sphingosine-1 phosphate-induced EC barrier enhancement. Phosphorylation of a conserved threonine ...
Source: AJP: Lung Cellular and Molecular Physiology - August 1, 2013 Category: Respiratory Medicine Authors: Adyshev, D. M., Dudek, S. M., Moldobaeva, N., Kim, K.-m., Ma, S.-F., Kasa, A., Garcia, J. G. N., Verin, A. D. Tags: ARTICLES Source Type: research
Lipoxin A4-mediated KATP potassium channel activation results in cystic fibrosis airway epithelial repair
The main cause of morbidity and mortality in cystic fibrosis (CF) is progressive lung destruction as a result of persistent bacterial infection and inflammation, coupled with reduced capacity for epithelial repair. Levels of the anti-inflammatory mediator lipoxin A4 (LXA4) have been reported to be reduced in bronchoalveolar lavages of patients with CF. We investigated the ability of LXA4 to trigger epithelial repair through the initiation of proliferation and migration in non-CF (NuLi-1) and CF (CuFi-1) airway epithelia. Spontaneous repair and cell migration were significantly slower in CF epithelial cultures (CuFi-1) comp...
Source: AJP: Lung Cellular and Molecular Physiology - July 15, 2013 Category: Respiratory Medicine Authors: Buchanan, P. J., McNally, P., Harvey, B. J., Urbach, V. Tags: ARTICLES Source Type: research
Efficient delivery of RNA interference oligonucleotides to polarized airway epithelia in vitro
Polarized and pseudostratified primary airway epithelia present barriers that significantly reduce their transfection efficiency and the efficacy of RNA interference oligonucleotides. This creates an impediment in studies of the airway epithelium, diminishing the utility of loss-of-function as a research tool. Here we outline methods to introduce RNAi oligonucleotides into primary human and porcine airway epithelia grown at an air-liquid interface and difficult-to-transfect transformed epithelial cell lines grown on plastic. At the time of plating, we reverse transfect small-interfering RNA (siRNA), Dicer-substrate siRNA, ...
Source: AJP: Lung Cellular and Molecular Physiology - July 1, 2013 Category: Respiratory Medicine Authors: Ramachandran, S., Krishnamurthy, S., Jacobi, A. M., Wohlford-Lenane, C., Behlke, M. A., Davidson, B. L., McCray, P. B. Tags: INNOVATIVE METHODOLOGY Source Type: research
LPS induces pp60c-src-mediated tyrosine phosphorylation of Hsp90 in lung vascular endothelial cells and mouse lung
Heat shock protein 90 (Hsp90) inhibitors were initially developed as anticancer agents; however, it is becoming increasing clear that they also possess potent anti-inflammatory properties. Posttranslational modifications of Hsp90 have been reported in tumors and have been hypothesized to affect client protein- and inhibitor-binding activities. In the present study we investigated the posttranslational modification of Hsp90 in inflammation. LPS, a prototypical inflammatory agent, induced concentration- and time-dependent tyrosine (Y) phosphorylation of Hsp90α and Hsp90β in bovine pulmonary arterial and human lung...
Source: AJP: Lung Cellular and Molecular Physiology - June 15, 2013 Category: Respiratory Medicine Authors: Barabutis, N., Handa, V., Dimitropoulou, C., Rafikov, R., Snead, C., Kumar, S., Joshi, A., Thangjam, G., Fulton, D., Black, S. M., Patel, V., Catravas, J. D. Tags: ARTICLES Source Type: research
Mechanical induction of group V phospholipase A2 causes lung inflammation and acute lung injury
This study tested the hypothesis that onset of VILI is triggered by activation of secretory group V phospholipase A2 (gVPLA2) in pulmonary vascular endothelium exposed to excessive mechanical stretch. High-magnitude cyclic stretch (18% CS) increased expression and surface exposure of gVPLA2 in human pulmonary endothelial cells (EC). CS-induced gVPLA2 activation was required for activation of ICAM-1 expression and polymorphonuclear neutrophil (PMN) adhesion to CS-preconditioned EC. By contrast, physiological CS (5% CS) had no effect on gVPLA2 activation or EC-PMN adhesion. CS-induced ICAM-1 expression and EC-PMN adhesion we...
Source: AJP: Lung Cellular and Molecular Physiology - May 15, 2013 Category: Respiratory Medicine Authors: Meliton, A. Y., Munoz, N. M., Meliton, L. N., Birukova, A. A., Leff, A. R., Birukov, K. G. Tags: ARTICLES Source Type: research
MARCKS and HSP70 interactions regulate mucin secretion by human airway epithelial cells in vitro
Myristoylated alanine-rich C kinase substrate (MARCKS) protein has been recognized as a key regulatory molecule controlling mucin secretion by airway epithelial cells in vitro and in vivo. We recently showed that two intracellular chaperones, heat shock protein 70 (HSP70) and cysteine string protein (CSP), associate with MARCKS in the secretory mechanism. To elucidate more fully MARCKS-HSP70 interactions in this process, studies were performed in well-differentiated normal human bronchial epithelial (NHBE) cells maintained in air-liquid interface culture utilizing specific pharmacological inhibition of HSP70 with pyrimidin...
Source: AJP: Lung Cellular and Molecular Physiology - April 15, 2013 Category: Respiratory Medicine Authors: Fang, S., Crews, A. L., Chen, W., Park, J., Yin, Q., Ren, X.-R., Adler, K. B. Tags: ARTICLES Source Type: research
Nicotine-induced epithelial-mesenchymal transition via Wnt/{beta}-catenin signaling in human airway epithelial cells
Epithelial-mesenchymal transition (EMT) has been proposed to be a mechanism in airway remodeling, which is a characteristic of chronic obstructive pulmonary disease (COPD). Studies have shown that cigarette smoke and nicotine are factors that induce Wnt/β-catenin activation, which is a pathway that has also been implicated in EMT. The main aim of this study was to test whether human bronchial epithelial cells are able to undergo EMT in vitro following nicotine stimulation via the Wnt3a/β-catenin signaling pathway. We show that nicotine activates the Wnt3a signal pathway, which leads to the translocation of β...
Source: AJP: Lung Cellular and Molecular Physiology - February 15, 2013 Category: Respiratory Medicine Authors: Zou, W., Zou, Y., Zhao, Z., Li, B., Ran, P. Tags: CALL FOR PAPERS Source Type: research
IL-13 receptor {alpha}2-arginase 2 pathway mediates IL-13-induced pulmonary hypertension
This study's goal was to investigate the role and mechanism of IL-13 in the pathogenesis of PH. Lung-specific IL-13-overexpressing transgenic (Tg) mice were examined for hemodynamic changes and pulmonary vascular remodeling. IL-13 Tg mice spontaneously developed PH phenotype by the age of 2 mo with increased expression and activity of arginase 2 (Arg2). The role of Arg2 in the development of IL-13-stimulated PH was further investigated using Arg2 and IL-13 receptor α2 (Rα2) null mutant mice and the small-interfering RNA (siRNA)-silencing approach in vivo and in vitro, respectively. IL-13-stimulated medial thick...
Source: AJP: Lung Cellular and Molecular Physiology - January 15, 2013 Category: Respiratory Medicine Authors: Cho, W.-K., Lee, C.-M., Kang, M.-J., Huang, Y., Giordano, F. J., Lee, P. J., Trow, T. K., Homer, R. J., Sessa, W. C., Elias, J. A., Lee, C. G. Tags: ARTICLES Source Type: research
