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10.1002/mc.22406 http://scihub22266oqcxt.onion/10.1002/mc.22406 C4794420!4794420 !26373456     free     free     free       Mol+Carcinog 2016 ; 55 (11 ): 1526-1541 Nephropedia Template TP {{tp|p=26373456 |t=2016. Autophagy levels are elevated in barrett s esophagus and promote cell survival from acid and oxidative stress |pdf=|usr=}}{{26373456 }} gab.com Text Autophagy levels are elevated in barrett s esophagus and promote cell survival from acid and oxidative stress JO: Mol Carcinog http://www.kidney.de/pget.php?&tw=1&pmid=26373456 #FOAvip Autophagy is a highly conserved mechanism that is activated during cellular stress. We hypothesized that autophagy may be induced by acid reflux, which causes injury, and inflammation, and therefore, contributes to the pathogenesis of Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). Currently, the role of autophagy in BE and EAC is poorly studied. We quantitatively define autophagy levels in human BE cell lines, a transgenic mouse model of BE, and human BE, and EAC biopsies. Human non-dysplastic BE had the highest basal number of autophagic vesicles (AVs), while AVs were reduced in normal squamous cells and dysplastic BE cells, and nearly absent in EAC. To demonstrate a functional role for autophagy in BE pathogenesis, normal squamous (STR), non-dysplastic BE (CPA), dysplastic BE (CPD), and EAC (OE19) cell lines were exposed to an acid pulse (pH?3.5) followed by incubation in the presence or absence of chloroquine, an autophagy inhibitor. Acid exposure increased reactive oxygen species (ROS) levels in STR and CPA cells. Chloroquine alone had a small impact on intracellular ROS or cell survival. However, combination of chloroquine with the acid pulse resulted in a significant increase in ROS levels at 6?h in STR and CPA cells, and increased cell death in all cell lines. These findings establish increased numbers of AVs in human BE compared to normal squamous or EAC, and suggest that autophagy functions to improve cell survival after acid reflux injury. Autophagy may thus play a critical role in BE pathogenesis and progression. © 2015 Wiley Periodicals, Inc. Twit Text FOAVip Autophagy levels are elevated in barrett s esophagus and promote cell survival from acid and oxidative stress ????Mol Carcinog http://www.kidney.de/pget.php?&tw=1&pmid=26373456 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26373456 #FOAvip English Wikipedia <ref>{{Cite pmid|26373456 }}</ref> Autophagy levels are elevated in barrett s esophagus and promote cell survival from acid and oxidative stress #MMPMID26373456 Kong J ; Whelan KA ; Laczkó D ; Dang B ; Caro Monroig A ; Soroush A ; Falcone J ; Amaravadi RK ; Rustgi AK ; Ginsberg GG ; Falk GW ; Nakagawa H ; Lynch JP Mol Carcinog 2016[Nov]; 55 (11 ): 1526-1541 PMID26373456 show ga Autophagy is a highly conserved mechanism that is activated during cellular stress. We hypothesized that autophagy may be induced by acid reflux, which causes injury, and inflammation, and therefore, contributes to the pathogenesis of Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). Currently, the role of autophagy in BE and EAC is poorly studied. We quantitatively define autophagy levels in human BE cell lines, a transgenic mouse model of BE, and human BE, and EAC biopsies. Human non-dysplastic BE had the highest basal number of autophagic vesicles (AVs), while AVs were reduced in normal squamous cells and dysplastic BE cells, and nearly absent in EAC. To demonstrate a functional role for autophagy in BE pathogenesis, normal squamous (STR), non-dysplastic BE (CPA), dysplastic BE (CPD), and EAC (OE19) cell lines were exposed to an acid pulse (pH?3.5) followed by incubation in the presence or absence of chloroquine, an autophagy inhibitor. Acid exposure increased reactive oxygen species (ROS) levels in STR and CPA cells. Chloroquine alone had a small impact on intracellular ROS or cell survival. However, combination of chloroquine with the acid pulse resulted in a significant increase in ROS levels at 6?h in STR and CPA cells, and increased cell death in all cell lines. These findings establish increased numbers of AVs in human BE compared to normal squamous or EAC, and suggest that autophagy functions to improve cell survival after acid reflux injury. Autophagy may thus play a critical role in BE pathogenesis and progression. © 2015 Wiley Periodicals, Inc. |Acids/*adverse effects [MESH] |Adenocarcinoma/metabolism/*pathology [MESH] |Animals [MESH] |Autophagy/drug effects [MESH] |Barrett Esophagus/metabolism/*pathology [MESH] |Cell Line [MESH] |Cell Survival [MESH] |Chloroquine/pharmacology [MESH] |Disease Models, Animal [MESH] |Disease Progression [MESH] |Esophageal Neoplasms/metabolism/*pathology [MESH] |Humans [MESH] |Mice [MESH] |Oxidative Stress [MESH]Autophagy levels are elevated in barrett s esophagus and promote cell (epmc).pdf DeepDyve Pubget Overpricing