Autophagy levels are elevated in barrett's esophagus and promote cell survival from acid and oxidative stress
Identifieur interne : 000E30 ( Main/Exploration ); précédent : 000E29; suivant : 000E31Autophagy levels are elevated in barrett's esophagus and promote cell survival from acid and oxidative stress
Auteurs : Jianping Kong [États-Unis] ; Kelly A. Whelan [États-Unis] ; Dorottya Laczk [États-Unis] ; Brendan Dang [États-Unis] ; Angeliz Caro Monroig [États-Unis] ; Ali Soroush [États-Unis] ; John Falcone [États-Unis] ; Ravi K. Amaravadi [États-Unis] ; Anil K. Rustgi [États-Unis] ; Gregory G. Ginsberg [États-Unis] ; Gary W. Falk [États-Unis] ; Hiroshi Nakagawa [États-Unis] ; John P. Lynch [États-Unis]Source :
- Molecular Carcinogenesis [ 0899-1987 ] ; 2016-11.
Abstract
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.
Url:
DOI: 10.1002/mc.22406
Affiliations:
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Lynch</name><affiliation wicri:level="3"><country>États-Unis</country><placeName><settlement type="city">Philadelphie</settlement><region type="state">Pennsylvanie</region></placeName><wicri:orgArea>Division of Gastroenterology, University of Pennsylvania, Pennsylvania</wicri:orgArea></affiliation><affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country></affiliation><affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Molecular Carcinogenesis</title><title level="j" type="alt">MOLECULAR CARCINOGENESIS</title><idno type="ISSN">0899-1987</idno><idno type="eISSN">1098-2744</idno><imprint><biblScope unit="vol">55</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="1526">1526</biblScope><biblScope unit="page" to="1541">1541</biblScope><biblScope unit="page-count">16</biblScope><date type="published" when="2016-11">2016-11</date></imprint><idno type="ISSN">0899-1987</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0899-1987</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Pennsylvanie</li></region><settlement><li>Philadelphie</li></settlement></list><tree><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Kong, Jianping" sort="Kong, Jianping" uniqKey="Kong J" first="Jianping" last="Kong">Jianping Kong</name></region><name sortKey="Amaravadi, Ravi K" sort="Amaravadi, Ravi K" uniqKey="Amaravadi R" first="Ravi K." last="Amaravadi">Ravi K. Amaravadi</name><name sortKey="Amaravadi, Ravi K" sort="Amaravadi, Ravi K" uniqKey="Amaravadi R" first="Ravi K." last="Amaravadi">Ravi K. Amaravadi</name><name sortKey="Caro Monroig, Angeliz" sort="Caro Monroig, Angeliz" uniqKey="Caro Monroig A" first="Angeliz" last="Caro Monroig">Angeliz Caro Monroig</name><name sortKey="Dang, Brendan" sort="Dang, Brendan" uniqKey="Dang B" first="Brendan" last="Dang">Brendan Dang</name><name sortKey="Falcone, John" sort="Falcone, John" uniqKey="Falcone J" first="John" last="Falcone">John Falcone</name><name sortKey="Falk, Gary W" sort="Falk, Gary W" uniqKey="Falk G" first="Gary W." last="Falk">Gary W. Falk</name><name sortKey="Ginsberg, Gregory G" sort="Ginsberg, Gregory G" uniqKey="Ginsberg G" first="Gregory G." last="Ginsberg">Gregory G. Ginsberg</name><name sortKey="Laczk, Dorottya" sort="Laczk, Dorottya" uniqKey="Laczk D" first="Dorottya" last="Laczk">Dorottya Laczk</name><name sortKey="Lynch, John P" sort="Lynch, John P" uniqKey="Lynch J" first="John P." last="Lynch">John P. Lynch</name><name sortKey="Lynch, John P" sort="Lynch, John P" uniqKey="Lynch J" first="John P." last="Lynch">John P. Lynch</name><name sortKey="Nakagawa, Hiroshi" sort="Nakagawa, Hiroshi" uniqKey="Nakagawa H" first="Hiroshi" last="Nakagawa">Hiroshi Nakagawa</name><name sortKey="Rustgi, Anil K" sort="Rustgi, Anil K" uniqKey="Rustgi A" first="Anil K." last="Rustgi">Anil K. Rustgi</name><name sortKey="Soroush, Ali" sort="Soroush, Ali" uniqKey="Soroush A" first="Ali" last="Soroush">Ali Soroush</name><name sortKey="Whelan, Kelly A" sort="Whelan, Kelly A" uniqKey="Whelan K" first="Kelly A." last="Whelan">Kelly A. Whelan</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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