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10.1152/ajplung.00250.2011 http://scihub22266oqcxt.onion/10.1152/ajplung.00250.2011 21926263!3233830!21926263     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Lung+Cell+Mol+Physiol 2011 ; 301 (6): L993-L1002 Nephropedia Template TP {{tp|p=21926263|t=2011. Activation of hypoxia-inducible factor-1 protects airway epithelium against oxidant-induced barrier dysfunction |pdf=|usr=}}{{21926263}} gab.com Text Activation of hypoxia-inducible factor-1 protects airway epithelium against oxidant-induced barrier dysfunction JO: Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=21926263 #FOAvip The respiratory epithelium forms an important barrier against inhaled pollutants and microorganisms, and its barrier function is often compromised during inflammatory airway diseases. Epithelial activation of hypoxia-inducible factor-1 (HIF-1) represents one feature of airway inflammation, but the functional importance of HIF-1 within the respiratory epithelium is largely unknown. Using primary mouse tracheal epithelial (MTE) cells or immortalized human bronchial epithelial cells (16HBE14o-), we evaluated the impact of HIF-1 activation on loss of epithelial barrier function during oxidative stress. Exposure of either 16HBE14o- or MTE cells to H(2)O(2) resulted in significant loss of transepithelial electrical resistance and increased permeability to fluorescein isothiocyanate-dextran (4 kDa), and this was attenuated significantly after prior activation of HIF-1 by preexposure to hypoxia (2% O(2); 6 h) or the hypoxia mimics CoCl(2) or dimethyloxalylglycine (DMOG). Oxidative barrier loss was associated with reduced levels of the tight junction protein occludin and with hyperoxidation of the antioxidant enzyme peroxiredoxin (Prx-SO(2)H), events that were also attenuated by prior activation of HIF-1. Involvement of HIF-1 in these protective effects was confirmed using the pharmacological inhibitor YC-1 and by short-hairpin RNA knockdown of HIF-1alpha. The protective effects of HIF-1 were associated with induction of sestrin-2, a hypoxia-inducible enzyme known to reduce oxidative stress and minimize Prx hyperoxidation. Together, our results suggest that loss of epithelial barrier integrity by oxidative stress is minimized by activation of HIF-1, in part by induction of sestrin-2. Twit Text FOAVip Activation of hypoxia-inducible factor-1 protects airway epithelium against oxidant-induced barrier dysfunction ????Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=21926263 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21926263 #FOAvip English Wikipedia <ref>{{Cite pmid|21926263}}</ref> Activation of hypoxia-inducible factor-1 protects airway epithelium against oxidant-induced barrier dysfunction #MMPMID21926263 Olson N; Hristova M; Heintz NH; Lounsbury KM; van der Vliet A Am J Physiol Lung Cell Mol Physiol 2011[Dec]; 301 (6): L993-L1002 PMID21926263show ga The respiratory epithelium forms an important barrier against inhaled pollutants and microorganisms, and its barrier function is often compromised during inflammatory airway diseases. Epithelial activation of hypoxia-inducible factor-1 (HIF-1) represents one feature of airway inflammation, but the functional importance of HIF-1 within the respiratory epithelium is largely unknown. Using primary mouse tracheal epithelial (MTE) cells or immortalized human bronchial epithelial cells (16HBE14o-), we evaluated the impact of HIF-1 activation on loss of epithelial barrier function during oxidative stress. Exposure of either 16HBE14o- or MTE cells to H(2)O(2) resulted in significant loss of transepithelial electrical resistance and increased permeability to fluorescein isothiocyanate-dextran (4 kDa), and this was attenuated significantly after prior activation of HIF-1 by preexposure to hypoxia (2% O(2); 6 h) or the hypoxia mimics CoCl(2) or dimethyloxalylglycine (DMOG). Oxidative barrier loss was associated with reduced levels of the tight junction protein occludin and with hyperoxidation of the antioxidant enzyme peroxiredoxin (Prx-SO(2)H), events that were also attenuated by prior activation of HIF-1. Involvement of HIF-1 in these protective effects was confirmed using the pharmacological inhibitor YC-1 and by short-hairpin RNA knockdown of HIF-1alpha. The protective effects of HIF-1 were associated with induction of sestrin-2, a hypoxia-inducible enzyme known to reduce oxidative stress and minimize Prx hyperoxidation. Together, our results suggest that loss of epithelial barrier integrity by oxidative stress is minimized by activation of HIF-1, in part by induction of sestrin-2. |Amino Acids, Dicarboxylic/pharmacology[MESH] |Animals[MESH] |Cell Hypoxia[MESH] |Cell Line[MESH] |Cobalt/pharmacology[MESH] |Dextrans/pharmacokinetics[MESH] |Fluorescein-5-isothiocyanate/analogs & derivatives/pharmacokinetics[MESH] |Fluorescent Dyes/pharmacokinetics[MESH] |Gene Knockdown Techniques[MESH] |Humans[MESH] |Hydrogen Peroxide/*pharmacology[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & inhibitors/*metabolism[MESH] |Membrane Proteins/metabolism[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Nuclear Proteins/metabolism[MESH] |Occludin[MESH] |Oxidants/*pharmacology[MESH] |Oxidation-Reduction[MESH] |Oxidative Stress[MESH] |Permeability[MESH] |Peroxiredoxins/metabolism[MESH] |Primary Cell Culture[MESH] |Procollagen-Proline Dioxygenase/antagonists & inhibitors[MESH] |RNA Interference[MESH] |Respiratory Mucosa/metabolism/*pathology[MESH]Activation of hypoxia-inducible factor-1 protects airway epithelium ag(epmc).pdf DeepDyve Pubget Overpricing