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10.1093/toxsci/kft253 http://scihub22266oqcxt.onion/10.1093/toxsci/kft253 24218148!3908723!24218148     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Toxicol+Sci 2014 ; 137 (2): 447-57 Nephropedia Template TP {{tp|p=24218148|t=2014. Loss of hypoxia-inducible factor 2 alpha in the lung alveolar epithelium of mice leads to enhanced eosinophilic inflammation in cobalt-induced lung injury |pdf=|usr=}}{{24218148}} gab.com Text Loss of hypoxia-inducible factor 2 alpha in the lung alveolar epithelium of mice leads to enhanced eosinophilic inflammation in cobalt-induced lung injury JO: Toxicol Sci http://www.kidney.de/pget.php?&tw=1&pmid=24218148 #FOAvip Hard metal lung disease (HMLD) is an occupational lung disease specific to inhalation of cobalt-containing particles whose mechanism is largely unknown. Cobalt is a known hypoxia mimic and stabilizer of the alpha subunits of hypoxia-inducible factors (HIFs). Previous work revealed that though HIF1alpha contrib utes to cobalt toxicity in vitro, loss of HIF1alpha in the alveolar epithelial cells does not provide in vivo protection from cobalt-induced lung inflammation. HIF1alpha and HIF2alpha show unique tissue expression profiles, and HIF2alpha is known to be the predominant HIF mRNA isoform in the adult lung. Thus, if HIF2alpha activation by cobalt contributes to pathophysiology of HMLD, we hypothesized that loss of HIF2alpha in lung epithelium would provide protection from cobalt-induced inflammation. Mice with HIF2alpha-deficiency in Club and alveolar type II epithelial cells (ATIIs) (HIF2alpha(Delta/Delta)) were exposed to cobalt (60 microg/day) or saline using a subacute occupational exposure model. Bronchoalveolar lavage cellularity, cytokines, qRT-PCR, and histopathology were analyzed. Results show that loss of HIF2alpha leads to enhanced eosinophilic inflammation and increased goblet cell metaplasia. Additionally, control mice demonstrated a mild recovery from cobalt-induced lung injury compared with HIF2alpha(Delta/Delta) mice, suggesting a role for epithelial HIF2alpha in repair mechanisms. The expression of important cytokines, such as interleukin (IL)-5 and IL-10, displayed significant differences following cobalt exposure when HIF2alpha(Delta/Delta) and control mice were compared. In summary, our data suggest that although loss of HIF2alpha does not afford protection from cobalt-induced lung inflammation, epithelial HIF2alpha signaling does play an important role in modulating the inflammatory and repair response in the lung. Twit Text FOAVip Loss of hypoxia-inducible factor 2 alpha in the lung alveolar epithelium of mice leads to enhanced eosinophilic inflammation in cobalt-induced lung injury ????Toxicol Sci http://www.kidney.de/pget.php?&tw=1&pmid=24218148 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24218148 #FOAvip English Wikipedia <ref>{{Cite pmid|24218148}}</ref> Loss of hypoxia-inducible factor 2 alpha in the lung alveolar epithelium of mice leads to enhanced eosinophilic inflammation in cobalt-induced lung injury #MMPMID24218148 Proper SP; Saini Y; Greenwood KK; Bramble LA; Downing NJ; Harkema JR; Lapres JJ Toxicol Sci 2014[Feb]; 137 (2): 447-57 PMID24218148show ga Hard metal lung disease (HMLD) is an occupational lung disease specific to inhalation of cobalt-containing particles whose mechanism is largely unknown. Cobalt is a known hypoxia mimic and stabilizer of the alpha subunits of hypoxia-inducible factors (HIFs). Previous work revealed that though HIF1alpha contrib utes to cobalt toxicity in vitro, loss of HIF1alpha in the alveolar epithelial cells does not provide in vivo protection from cobalt-induced lung inflammation. HIF1alpha and HIF2alpha show unique tissue expression profiles, and HIF2alpha is known to be the predominant HIF mRNA isoform in the adult lung. Thus, if HIF2alpha activation by cobalt contributes to pathophysiology of HMLD, we hypothesized that loss of HIF2alpha in lung epithelium would provide protection from cobalt-induced inflammation. Mice with HIF2alpha-deficiency in Club and alveolar type II epithelial cells (ATIIs) (HIF2alpha(Delta/Delta)) were exposed to cobalt (60 microg/day) or saline using a subacute occupational exposure model. Bronchoalveolar lavage cellularity, cytokines, qRT-PCR, and histopathology were analyzed. Results show that loss of HIF2alpha leads to enhanced eosinophilic inflammation and increased goblet cell metaplasia. Additionally, control mice demonstrated a mild recovery from cobalt-induced lung injury compared with HIF2alpha(Delta/Delta) mice, suggesting a role for epithelial HIF2alpha in repair mechanisms. The expression of important cytokines, such as interleukin (IL)-5 and IL-10, displayed significant differences following cobalt exposure when HIF2alpha(Delta/Delta) and control mice were compared. In summary, our data suggest that although loss of HIF2alpha does not afford protection from cobalt-induced lung inflammation, epithelial HIF2alpha signaling does play an important role in modulating the inflammatory and repair response in the lung. |Animals[MESH] |Basic Helix-Loop-Helix Transcription Factors/*deficiency/genetics[MESH] |Bronchoalveolar Lavage Fluid/cytology[MESH] |Cobalt/*toxicity[MESH] |Cytokines/genetics/immunology[MESH] |Disease Models, Animal[MESH] |Doxycycline/pharmacology[MESH] |Gene Expression Profiling[MESH] |Immunohistochemistry[MESH] |Lung Injury/*chemically induced/complications/immunology/pathology[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Pulmonary Alveoli/*drug effects/immunology/pathology[MESH] |Pulmonary Eosinophilia/*chemically induced/etiology/immunology/pathology[MESH]Loss of hypoxia-inducible factor 2 alpha in the lung alveolar epitheli(epmc).pdf DeepDyve Pubget Overpricing