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Peroxisome Proliferator-Activated Receptor Gamma Enhances Human Pulmonary Artery Smooth Muscle Cell Apoptosis Through MicroRNA-21 and Programmed Cell Death 4.
Abstract Pulmonary hypertension (PH) is a progressive disorder whose cellular pathogenesis involves enhanced smooth muscle cell (SMC) proliferation and resistance to apoptosis signals. Existing evidence demonstrates that the tumor suppressor, programmed cell death 4 (PDCD4) affects patterns of cell growth and repair responses in the systemic vasculature following experimental injury. In the current study, the regulation PDCD4 and its functional effects on growth and apoptosis susceptibility in pulmonary artery smooth muscle cells was explored. We previously demonstrated that pharmacological activation of the nucle...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - May 18, 2017 Category: Cytology Authors: Green DE, Murphy TC, Kang BY, Bedi B, Yuan Z, Sadikot RT, Hart CM Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Estrogen and cigarette sidestream smoke particulate matter exhibit ER α-dependent tumor-promoting effects in lung adenocarcinoma cells.
This study demonstrates that estrogen has ERα-dependent tumor-promoting activity. CSSP acts like estrogen and shows a potential to enhance estrogen-induced ERα action. PMID: 28522562 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - May 18, 2017 Category: Cytology Authors: Kuo LC, Cheng LC, Lee CH, Lin CJ, Chen PY, Li LA Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Autophagy Plays a Role in FSTL1-induced EMT and Airway Remodeling in Asthma.
In this study, we hypothesized that Follistatin-like 1(FSTL1) promotes EMT and airway remodeling by intensifying autophagy. Using transmission electron microscopy (TEM), double membrane autophagosomes were detected in the airways of patients and mice. More autophagosomes were in asthmatic patients and OVA-challenged mice compared to healthy control. The expression of FSTL1 and Beclin1 were upregulated in the airways of asthmatic patients and OVA-challenged mice, accompany with airway EMT and remodeling. In OVA-challenged Fstl1+/- mice, the degree of airway remodeling and autophagy were decreased compared to control mice. T...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - May 4, 2017 Category: Cytology Authors: Liu T, Liu Y, Miller M, Cao L, Zhao J, Wu J, Wang J, Liu L, Li S, Zou M, Xu J, Broide DH, Dong L Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Focal Adhesion Kinase Signaling Determines the Fate of Lung Epithelial Cells in Response to TGF- β.
In this report, we explore the role of focal adhesion kinase (FAK) signaling in determining the fate of lung epithelial cells in response to TGF-β1. Rat type II alveolar epithelial cells (RLE-6TN) were treated with or without TGF-β1, and the expression of mesenchymal phenotype and function were analyzed. Pharmacologic protein kinase inhibitors were utilized to screen for SMAD-dependent and -independent pathways. SMAD and FAK signaling were analyzed using siRNA knockdown, inhibitors, and expression of mutant constructs of FAK. Apoptosis was measured using cleaved caspase-3 analysis and TUNEL staining. TGF-β1 induced the ...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - March 30, 2017 Category: Cytology Authors: Ding Q, Subramanian I, Luckhardt TR, Che P, Waghray M, Zhao X, Bone N, Kurundkar AR, Hecker L, Hu M, Zhou Y, Horowitz JC, Vittal R, Thannickal VJ Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Hypoxic proliferation requires EGFR-mediated ERK activation in human pulmonary microvascular endothelial cells.
Abstract We have previously shown that hypoxic proliferation of human pulmonary microvascular endothelial cells (hPMVEC) depends on epidermal growth factor receptor (EGFR) activation. To determine down-stream signaling leading to proliferation, we tested the hypothesis that hypoxia-induced proliferation in hPMVEC would require EGFR-mediated activation of extracellular signal-regulated kinase (ERK) leading to arginase II induction. To test this hypothesis, hPMVEC were incubated in either normoxia (21% O2, 5% CO2) or hypoxia (1% O2, 5% CO2) and western blotting was performed for EGFR, arginase II, phosphorylated-ERK...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - February 9, 2017 Category: Cytology Authors: White HA, Jin Y, Chicoine LG, Chen B, Liu Y, Nelin LD Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Ca2+/Calmodulin-Dependent Protein Kinase II β and IIδ Mediate TGFβ-Induced Transduction of Fibronectin and Collagen in Human Pulmonary Fibroblasts.
In this study, we examined the interactions between calcium signaling, activation of CamK and other kinases, and extracellular matrix (ECM) gene expression. Human pulmonary fibroblasts were cultured and stimulated with artificially-generated Ca2+-pulses in the absence of TGFβ, or with TGFβ (1 nM) or vehicle in the presence of various blockers of Ca2+ signaling. PCR and Western blotting were used to measure gene expression and protein levels, respectively. We found that Ca2+-pulses in the absence of TGFβ increased ECM gene expression in a pulse frequency-dependent manner, and that blocking Ca2+ signaling and the CamK II ...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - January 26, 2017 Category: Cytology Authors: Mukherjee S, Sheng W, Sun R, Janssen LJ Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Glucocorticoid and TNF signaling converge at A20 (TNFAIP3) to repress airway smooth muscle cytokine expression.
Abstract Airway smooth muscle is a major target tissue for glucocorticoid-based asthma therapies, however, molecular mechanisms through which the glucocorticoid receptor (GR) exerts therapeutic effects in this key airway cell type have not been fully elucidated. We previously identified the NF-kB inhibitor, A20 (TNFAIP3), as a mediator of cytokine repression by glucocorticoids (GCs) in airway epithelial cells and defined cooperative regulation of anti-inflammatory genes by GR and NF-kB as a key mechanistic underpinning of airway epithelial GR function. Here, we expand on these findings to determine whether a simil...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - June 30, 2016 Category: Cytology Authors: Sasse SK, Altonsy MO, Kadiyala V, Cao G, Panettieri RA, Gerber AN Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Chronic high magnitude cyclic stretch stimulates EC inflammatory response via VEGF Receptor 2 dependent mechanism.
This study demonstrates for the first time a VEGFR2-dependent mechanism of EC inflammatory activation induced by pathologic CS. We conclude that, despite the recognized role of VEGF as a pro-survival and angiogenic factor, excessive activation of VEGFR2 signaling by high tidal volume lung mechanical ventilation may contribute to ventilator-induced (biotrauma) lung inflammation and barrier dysfunction by augmenting cell response to VILI-associated inflammatory mediators. PMID: 26993523 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - March 18, 2016 Category: Cytology Authors: Gawlak G, Son S, Tian Y, O'Donnell JJ, Birukov KG, Birukova AA Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Pathogenic Role of Calcium-sensing Receptors in the Development and Progression of Pulmonary Hypertension.
Abstract An increase in [Ca(2+)]cyt in pulmonary arterial smooth muscle cells (PASMC) is a major trigger for pulmonary vasoconstriction and a critical stimulation for PASMC proliferation and migration. We previously demonstrated that expression and function of calcium sensing receptors (CaSR) in PASMC from patients with IPAH and animals with experimental PH were greater than in PASMC from normal subjects and control animals. However, the mechanisms by which CaSR triggers Ca(2+) influx in PASMC and the implication of CaSR in the development of PH remain elusive. Here we report that CaSR functionally interacts with ...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - March 11, 2016 Category: Cytology Authors: Tang H, Yamamura A, Yamamura H, Song S, Fraidenburg DR, Chen J, Gu Y, Pohl NM, Zhou T, Jiménez-Pérez L, Ayon RJ, Desai AA, Goltzman D, Rischard F, Khalpey ZI, Black SM, Garcia JG, Makino A, Yuan JX Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

The Src family tyrosine kinases, src and yes, have differential effects on inflammation-induced apoptosis in human pulmonary microvascular endothelial cells.
Abstract Endothelial cells are essential for normal lung function by sensing and responding to circulating factors and hemodynamic alterations. In inflammatory lung diseases, like acute respiratory distress syndrome (ARDS), endothelial cell apoptosis is an inciting event in pathogenesis and a prominent pathological feature. Endothelial cell apoptosis is mediated by circulating inflammatory factors, which bind to receptors on the cell surface activating signal transduction pathways leading to caspase 3-mediated apoptosis. We hypothesized that yes and src have differential effects on caspase 3 activation in human pu...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - February 26, 2016 Category: Cytology Authors: Nelin LD, White HA, Jin Y, Trittmann JK, Chen B, Liu Y Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Targeting host calpain proteases decreases influenza A virus infection.
Abstract 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 to diverse cellular responses, including inflammation. Here, we used in vitro and in vivo approaches to investigate the role of calpains signalling in IAV pathogenesis. Calpain expression and activity were found altered in IAV-infected bronchial epithelial cells. Using siRNA gene silencing, specific synth...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - January 8, 2016 Category: Cytology Authors: Blanc F, Furio L, Moisy D, Yen HL, Chignard M, Letavernier E, Naffakh N, Mok CK, Si-Tahar M Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

An Oxidative DNA "Damage" and Repair Mechanism Localized in the VEGF Promoter is Important for Hypoxia-induced VEGF mRNA Expression.
Abstract In hypoxia, mitochondria-generated reactive oxygen species (ROS) not only stimulate accumulation of the transcriptional regulator of hypoxic gene expression, Hif-1, but also cause oxidative base modifications in hypoxic response elements (HREs) of hypoxia-inducible genes. When the hypoxia-induced base modifications are suppressed, Hif-1 fails to associate with the HRE of the VEGF promoter and VEGF mRNA accumulation is blunted. The mechanism linking base modifications to transcription is unknown. Here we determined if recruitment of base excision DNA repair (BER) enzymes in response to hypoxia-induced prom...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - October 2, 2015 Category: Cytology Authors: Pastukh VM, Roberts J, Clark DW, Bardwell GC, Patel M, Al-Mehdi AB, Borchert G, Gillespie MN Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Pharmacologic inhibition of lactate production prevents myofibroblast differentiation.
CONCLUSIONS: Gossypol inhibits TGF-β induced myofibroblast differentiation through inhibition of LDH, inhibition of extracellular accumulation of lactic acid and inhibition of TGF-β bioactivity. These data support the hypothesis that pharmacologic inhibition of LDH may play an important role in the treatment of pulmonary fibrosis. PMID: 26408551 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - September 25, 2015 Category: Cytology Authors: Kottmann RM, Trawick E, Judge JL, Wahl LA, Epa A, Owens KM, Thatcher TH, Phipps RP, Sime PJ Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Leptin Enhances ICAM-1 Expression, Induces Migration and Cytokine Synthesis, and Prolongs Survival of Human Airway Epithelial Cells.
Abstract There is rising interest in how obesity affects respiratory diseases, since epidemiological findings indicate a strong relationship between the two conditions. Leptin is a potent adipokine produced mainly by adipocytes. It regulates energy storage and expenditure and also induces inflammation. Previous studies have shown that leptin is able to activate inflammatory cells such as lymphocytes and granulocytes, but little is known about its effect on lung structural cells. The present study investigated the effects of leptin on human airway epithelial cells by using human primary airway epithelial cells and ...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - August 14, 2015 Category: Cytology Authors: Suzukawa M, Koketsu R, Baba S, Igarashi S, Nagase H, Yamaguchi M, Matsutani N, Kawamura M, Shoji S, Hebisawa A, Ohta K Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Neutral Sphingomyelinase 2 is Required for Cytokine Induced Skeletal Muscle Calpain Activation.
CONCLUSIONS: These data suggest that nSMase2 activation is required for the development of infection-induced diaphragm calpain activation and muscle weakness. As a consequence, therapies that inhibit nSMase2 in patients may prevent infection-induced skeletal muscle dysfunction. PMID: 26138644 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - July 2, 2015 Category: Cytology Authors: Supinski GS, Alimov AP, Wang L, Song XH, Callahan LA Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

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