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Source: AJP: Lung Cellular and Molecular Physiology
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Total 59 results found since Jan 2013.
Pulmonary artery smooth muscle cell endothelin-1 expression modulates the pulmonary vascular response to chronic hypoxia
Endothelin-1 (ET-1) increases pulmonary vascular tone through direct effects on pulmonary artery smooth muscle cells (PASMC) via membrane-bound ET-1 receptors. Circulating ET-1 contributes to vascular remodeling by promoting SMC proliferation and migration and inhibiting SMC apoptosis. Although endothelial cells (EC) are the primary source of ET-1, whether ET-1 produced by SMC modulates pulmonary vascular tone is unknown. Using transgenic mice created by crossbreeding SM22α-Cre mice with ET-1 flox/flox mice to selectively delete ET-1 in SMC, we tested the hypothesis that PASMC ET-1 gene expression modulates the pulmo...
Source: AJP: Lung Cellular and Molecular Physiology - February 15, 2015 Category: Respiratory Medicine Authors: Kim, F. Y., Barnes, E. A., Ying, L., Chen, C., Lee, L., Alvira, C. M., Cornfield, D. N. Tags: CALL FOR PAPERS Source Type: research
Differential and opposing effects of imatinib on LPS- and ventilator-induced lung injury
Endothelial dysfunction underlies the pathophysiology of vascular disorders such as acute lung injury (ALI) syndromes. Recent work has identified the Abl family kinases (c-Abl and Arg) as important regulators of endothelial cell (EC) barrier function and suggests that their inhibition by currently available pharmaceutical agents such as imatinib may be EC protective. Here we describe novel and differential effects of imatinib in regulating lung pathophysiology in two clinically relevant experimental models of ALI. Imatinib attenuates endotoxin (LPS)-induced vascular leak and lung inflammation in mice but exacerbates these ...
Source: AJP: Lung Cellular and Molecular Physiology - February 1, 2015 Category: Respiratory Medicine Authors: Letsiou, E., Rizzo, A. N., Sammani, S., Naureckas, P., Jacobson, J. R., Garcia, J. G. N., Dudek, S. M. Tags: CALL FOR PAPERS Source Type: research
Nox2-dependent glutathionylation of endothelial NOS leads to uncoupled superoxide production and endothelial barrier dysfunction in acute lung injury
This study was designed to investigate how eNOS-dependent superoxide production contributes to endothelial barrier dysfunction in inflammatory lung injury and its regulation. C57BL/6J mice were challenged with intratracheal LPS. Bronchoalveolar lavage fluid was analyzed for protein accumulation, and lung tissue homogenate was assayed for endothelial NOS content and function. Human lung microvascular endothelial cell (HLMVEC) monolayers were exposed to LPS in vitro, and barrier integrity and superoxide production were measured. Biopterin species were quantified, and coimmunoprecipitation (Co-IP) assays were performed to ide...
Source: AJP: Lung Cellular and Molecular Physiology - December 15, 2014 Category: Respiratory Medicine Authors: Wu, F., Szczepaniak, W. S., Shiva, S., Liu, H., Wang, Y., Wang, L., Wang, Y., Kelley, E. E., Chen, A. F., Gladwin, M. T., McVerry, B. J. Tags: ARTICLES Source Type: research
Dicer mediating the expression of miR-143 and miR-155 regulates hexokinase II associated cellular response to hypoxia
Lung alveolar epithelial cells are exposed to hypoxia under a variety of physiological and pathological conditions. It has been shown recently that miR-143, which can directly target the key glycolytic enzyme hexokinase II (HK2), may be regulated by miR-155. We investigated whether microRNAs contribute to the cellular glycolysis in response to hypoxia. Using the A549 cells, we found that the expression of Dicer is decreased under hypoxia. When Dicer was knocked down with small-interfering RNA (siRNA), pre-miR143 was increased and mature miR-143 was decreased as that in hypoxia, indicating that reduction of Dicer is respons...
Source: AJP: Lung Cellular and Molecular Physiology - December 1, 2014 Category: Respiratory Medicine Authors: Yao, M., Wang, X., Tang, Y., Zhang, W., Cui, B., Liu, Q., Xing, L. Tags: CALL FOR PAPERS Source Type: research
GSK3{beta}-dependent inhibition of AMPK potentiates activation of neutrophils and macrophages and enhances severity of acute lung injury
Although AMP-activated protein kinase (AMPK) is involved in regulating carbohydrate and lipid metabolism, activated AMPK also plays an anti-inflammatory role in many cell populations. However, despite the ability of AMPK activation to diminish the severity of inflammatory responses, previous studies have found that AMPK activity is diminished in LPS-treated neutrophils and also in lungs of mice with LPS-induced acute lung injury (ALI). Since GSK3β participates in regulating AMPK activity, we examined potential roles for GSK3β in modulating LPS-induced activation of neutrophils and macrophages and in influencing s...
Source: AJP: Lung Cellular and Molecular Physiology - November 15, 2014 Category: Respiratory Medicine Authors: Park, D. W., Jiang, S., Liu, Y., Siegal, G. P., Inoki, K., Abraham, E., Zmijewski, J. W. Tags: CALL FOR PAPERS Source Type: research
Impaired TLR4 and HIF expression in cystic fibrosis bronchial epithelial cells downregulates hemeoxygenase-1 and alters iron homeostasis in vitro
In this study, we investigated in vitro the role of Toll-like receptor 4 (TLR4), hypoxia-inducible factor 1α (HIF-1α), and iron on HO-1 expression in cystic fibrosis (CF). Immunohistochemical analysis of TLR4, HO-1, ferritin, and HIF-1α were performed on lung sections of CFTR–/– and wild-type mice. CFBE41o- and 16HBE14o- cell lines were employed for in vitro analysis via immunoblotting, immunofluorescence, real-time PCR, luciferase reporter gene analysis, and iron quantification. We observed a reduced TLR4, HIF-1α, HO-1, and ferritin in CFBE41o- cell line and CF mice. Knockdown studies u...
Source: AJP: Lung Cellular and Molecular Physiology - November 15, 2014 Category: Respiratory Medicine Authors: Chillappagari, S., Venkatesan, S., Garapati, V., Mahavadi, P., Munder, A., Seubert, A., Sarode, G., Guenther, A., Schmeck, B. T., Tummler, B., Henke, M. O. Tags: ARTICLES Source Type: research
Silencing Bruton's tyrosine kinase in alveolar neutrophils protects mice from LPS/immune complex-induced acute lung injury
In conclusion, we put forward a hypothesis that Btk-targeted neutrophil specific therapy is a valid goal of research geared toward restoring homeostasis in lungs of patients with ALI/ARDS.
Source: AJP: Lung Cellular and Molecular Physiology - September 15, 2014 Category: Respiratory Medicine Authors: Krupa, A., Fol, M., Rahman, M., Stokes, K. Y., Florence, J. M., Leskov, I. L., Khoretonenko, M. V., Matthay, M. A., Liu, K. D., Calfee, C. S., Tvinnereim, A., Rosenfield, G. R., Kurdowska, A. K. Tags: CALL FOR PAPERS Source Type: research
Promotion of lung tumor growth by interleukin-17
Recent findings demonstrate that inhaled cigarette smoke, the predominant lung carcinogen, elicits a T helper 17 (Th17) inflammatory phenotype. Interleukin-17A (IL-17), the hallmark cytokine of Th17 inflammation, displays pro- and antitumorigenic properties in a manner that varies according to tumor type and assay system. To investigate the role of IL-17 in lung tumor growth, we used an autochthonous tumor model (K-RasLA1 mice) with lung delivery of a recombinant adenovirus that expresses IL-17A. Virus-mediated expression of IL-17A in K-RasLA1 mice at 8–10 wk of age doubled lung tumor growth in 3 wk relative to litte...
Source: AJP: Lung Cellular and Molecular Physiology - September 15, 2014 Category: Respiratory Medicine Authors: Xu, B., Guenther, J. F., Pociask, D. A., Wang, Y., Kolls, J. K., You, Z., Chandrasekar, B., Shan, B., Sullivan, D. E., Morris, G. F. Tags: ARTICLES Source Type: research
Fibroblasts that resist cigarette smoke-induced senescence acquire profibrotic phenotypes
This study assessed the effect of extended exposure to cigarette smoke extract (CSE) on tissue repair functions in lung fibroblasts. Human fetal (HFL-1) and adult lung fibroblasts were exposed to CSE for 14 days. Senescence-associated β-galactosidase (SA β-gal) expression, cell proliferation, and tissue repair functions including chemotaxis and gel contraction were assessed. HFL-1 proliferation was inhibited by CSE and nearly half of the CSE-exposed cells were SA β-gal positive after 14 days exposure, whereas 33% of adult lung fibroblasts were SA β-gal positive in response to 10% CSE exposure. The SA &b...
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2014 Category: Respiratory Medicine Authors: Kanaji, N., Basma, H., Nelson, A., Farid, M., Sato, T., Nakanishi, M., Wang, X., Michalski, J., Li, Y., Gunji, Y., Feghali-Bostwick, C., Liu, X., Rennard, S. I. Tags: ARTICLES Source Type: research
Matrix metalloproteinase-9 activates TGF-{beta} and stimulates fibroblast contraction of collagen gels
This study provides direct evidence that endogenously produced MMP-9 has a role in regulation of tissue contraction of 3D collagen gels mediated by fibroblasts.
Source: AJP: Lung Cellular and Molecular Physiology - June 1, 2014 Category: Respiratory Medicine Authors: Kobayashi, T., Kim, H., Liu, X., Sugiura, H., Kohyama, T., Fang, Q., Wen, F.-Q., Abe, S., Wang, X., Atkinson, J. J., Shipley, J. M., Senior, R. M., Rennard, S. I. Tags: ARTICLES Source Type: research
TNF-{alpha} induces cytosolic phospholipase A2 expression via Jak2/PDGFR-dependent Elk-1/p300 activation in human lung epithelial cells
Cytosolic phospholipase A2 (cPLA2) plays a pivotal role in mediating agonist-induced arachidonic acid release for prostaglandin (PG) synthesis during inflammation triggered by tumor necrosis factor-α (TNF-α). However, the mechanisms underlying TNF-α-induced cPLA2 expression in human lung epithelial cells (HPAEpiCs) were not completely understood. Here, we demonstrated that TNF-α induced cPLA2 mRNA and protein expression, promoter activity, and PGE2 secretion in HPAEpiCs. These responses induced by TNF-α were inhibited by pretreatment with the inhibitor of Jak2 (AG490), platelet-derived growth ...
Source: AJP: Lung Cellular and Molecular Physiology - March 15, 2014 Category: Respiratory Medicine Authors: Yang, C.-M., Lee, I.-T., Chi, P.-L., Cheng, S.-E., Hsiao, L.-D., Hsu, C.-K. Tags: ARTICLES Source Type: research
Transgelin as a therapeutic target to prevent hypoxic pulmonary hypertension
We previously observed that transgelin was preferentially expressed in human pulmonary arterial smooth muscle cells (PAMSCs) under hypoxia and that the upregulation of transgelin was independent of hypoxia-inducible factor 1α (HIF-1α). Reduced transgelin expression was accompanied by significantly impaired migration ability in vitro. However, the regulation mechanism of transgelin and its function in preventing hypoxic pulmonary hypertension (HPH) was unclear. In the present study, RNA interference with hypoxia-inducible factor 2α (HIF-2α) was employed in human PASMCs. Transgelin expression was dimi...
Source: AJP: Lung Cellular and Molecular Physiology - March 15, 2014 Category: Respiratory Medicine Authors: Zhang, R., Shi, L., Zhou, L., Zhang, G., Wu, X., Shao, F., Ma, G., Ying, K. Tags: ARTICLES Source Type: research
Nox2/ROS-dependent human antigen R translocation contributes to TNF-{alpha}-induced SOCS-3 expression in human tracheal smooth muscle cells
Elevated levels of TNF-α have been detected in the airway fluids, which may induce upregulation of inflammatory proteins. Suppressors of cytokine signaling (SOCS)-3 proteins can be induced by various cytokines and negatively regulated inflammatory responses. Although TNF-α has been shown to induce SOCS-3 expression, the mechanisms underlying TNF-α-induced SOCS-3 expression in human tracheal smooth muscle cells (HTSMCs) remain unclear. Here, we showed that TNF-α induced SOCS-3 expression, which was inhibited by pretreatment with the inhibitor of transcription level (actinomycin D), translation level ...
Source: AJP: Lung Cellular and Molecular Physiology - March 15, 2014 Category: Respiratory Medicine Authors: Hsu, C.-K., Lee, I.-T., Lin, C.-C., Hsiao, L.-D., Yang, C.-M. Tags: ARTICLES Source Type: research
The p66Shc adapter protein regulates the morphogenesis and epithelial maturation of fetal mouse lungs
Many signaling pathways are mediated by Shc adapter proteins that, in turn, are expressed as three isoforms with distinct functions. The p66Shc isoform antagonizes proliferation, regulates oxidative stress, and mediates apoptosis. It is highly expressed in the canalicular but not the later stages of mouse lung development, and its expression persists in bronchopulmonary dysplasia, a chronic disease associated with premature birth. These observations suggest that p66Shc has a developmental function. However, constitutive p66Shc deletion yields no morphological phenotype, and the structure of the Shc gene precludes its induc...
Source: AJP: Lung Cellular and Molecular Physiology - February 15, 2014 Category: Respiratory Medicine Authors: Lee, M. K., Smith, S. M., Banerjee, M. M., Li, C., Minoo, P., Volpe, M. V., Nielsen, H. C. Tags: ARTICLES Source Type: research
Inducible HSP70 regulates superoxide dismutase-2 and mitochondrial oxidative stress in the endothelial cells from developing lungs
Superoxide dismutase 2 (SOD-2) is synthesized in the cytosol and imported into the mitochondrial matrix, where it is activated and functions as the primary antioxidant for cellular respiration. The specific mechanisms that target SOD-2 to the mitochondria remain unclear. We hypothesize that inducible heat shock protein 70 (iHSP70) targets SOD-2 to the mitochondria via a mechanism facilitated by ATP, and this process is impaired in persistent pulmonary hypertension of the newborn (PPHN). We observed that iHSP70 interacts with SOD-2 and targets SOD-2 to the mitochondria. Interruption of iHSP70-SOD-2 interaction with 2-phenyl...
Source: AJP: Lung Cellular and Molecular Physiology - February 15, 2014 Category: Respiratory Medicine Authors: Afolayan, A. J., Teng, R.-J., Eis, A., Rana, U., Broniowska, K. A., Corbett, J. A., Pritchard, K., Konduri, G. G. Tags: ARTICLES Source Type: research
