Autophagy levels are elevated in barrett's esophagus and promote cell survival from acid and oxidative stress
Identifieur interne : 000156 ( Istex/Corpus ); précédent : 000155; suivant : 000157Autophagy levels are elevated in barrett's esophagus and promote cell survival from acid and oxidative stress
Auteurs : Jianping Kong ; Kelly A. Whelan ; Dorottya Laczk ; Brendan Dang ; Angeliz Caro Monroig ; Ali Soroush ; John Falcone ; Ravi K. Amaravadi ; Anil K. Rustgi ; Gregory G. Ginsberg ; Gary W. Falk ; Hiroshi Nakagawa ; John P. LynchSource :
- 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.
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DOI: 10.1002/mc.22406
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Amaravadi</name><affiliation><mods:affiliation>Division of Hematology/Oncology, University of Pennsylvania, Philadelphia, Pennsylvania</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Medicine, and the Abramson Cancer Center, University of Pennsylvania, Pennsylvania, Philadelphia</mods:affiliation></affiliation></author><author><name sortKey="Rustgi, Anil K" sort="Rustgi, Anil K" uniqKey="Rustgi A" first="Anil K." last="Rustgi">Anil K. Rustgi</name><affiliation><mods:affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</mods:affiliation></affiliation></author><author><name sortKey="Ginsberg, Gregory G" sort="Ginsberg, Gregory G" uniqKey="Ginsberg G" first="Gregory G." last="Ginsberg">Gregory G. Ginsberg</name><affiliation><mods:affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</mods:affiliation></affiliation></author><author><name sortKey="Falk, Gary W" sort="Falk, Gary W" uniqKey="Falk G" first="Gary W." last="Falk">Gary W. Falk</name><affiliation><mods:affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</mods:affiliation></affiliation></author><author><name sortKey="Nakagawa, Hiroshi" sort="Nakagawa, Hiroshi" uniqKey="Nakagawa H" first="Hiroshi" last="Nakagawa">Hiroshi Nakagawa</name><affiliation><mods:affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</mods:affiliation></affiliation></author><author><name sortKey="Lynch, John P" sort="Lynch, John P" uniqKey="Lynch J" first="John P." last="Lynch">John P. Lynch</name><affiliation><mods:affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: lynchj@mail.med.upenn.edu</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence to: Division of Gastroenterology/912 BRB II/III, 421 Curie Blvd., Philadelphia, PA. 19104.</mods: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><istex><corpusName>wiley</corpusName><author><json:item><name>Jianping Kong</name><affiliations><json:string>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</json:string></affiliations></json:item><json:item><name>Kelly A. Whelan</name><affiliations><json:string>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</json:string></affiliations></json:item><json:item><name>Dorottya Laczkó</name><affiliations><json:string>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</json:string></affiliations></json:item><json:item><name>Brendan Dang</name><affiliations><json:string>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</json:string></affiliations></json:item><json:item><name>Angeliz Caro Monroig</name><affiliations><json:string>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</json:string></affiliations></json:item><json:item><name>Ali Soroush</name><affiliations><json:string>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</json:string></affiliations></json:item><json:item><name>John Falcone</name><affiliations><json:string>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</json:string></affiliations></json:item><json:item><name>Ravi K. Amaravadi</name><affiliations><json:string>Division of Hematology/Oncology, University of Pennsylvania, Philadelphia, Pennsylvania</json:string><json:string>Department of Medicine, and the Abramson Cancer Center, University of Pennsylvania, Pennsylvania, Philadelphia</json:string></affiliations></json:item><json:item><name>Anil K. Rustgi</name><affiliations><json:string>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</json:string></affiliations></json:item><json:item><name>Gregory G. Ginsberg</name><affiliations><json:string>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</json:string></affiliations></json:item><json:item><name>Gary W. Falk</name><affiliations><json:string>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</json:string></affiliations></json:item><json:item><name>Hiroshi Nakagawa</name><affiliations><json:string>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</json:string></affiliations></json:item><json:item><name>John P. Lynch</name><affiliations><json:string>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</json:string><json:string>E-mail: lynchj@mail.med.upenn.edu</json:string><json:string>Correspondence to: Division of Gastroenterology/912 BRB II/III, 421 Curie Blvd., Philadelphia, PA. 19104.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Barrett's esophagus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>autophagy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>oxidative stress</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>esophageal adenocarcinoma</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>chloroquine</value></json:item></subject><articleId><json:string>MC22406</json:string></articleId><arkIstex>ark:/67375/WNG-LTDG2T7K-C</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><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.</abstract><qualityIndicators><score>10</score><pdfWordCount>8679</pdfWordCount><pdfCharCount>56327</pdfCharCount><pdfVersion>1.4</pdfVersion><pdfPageCount>16</pdfPageCount><pdfPageSize>595.276 x 790.866 pts</pdfPageSize><pdfWordsPerPage>542</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>250</abstractWordCount><abstractCharCount>1595</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Autophagy levels are elevated in barrett's esophagus and promote cell survival from acid and oxidative stress</title><genre><json:string>article</json:string></genre><host><title>Molecular 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SURVIVAL</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher ref="https://scientific-publisher.data.istex.fr/ark:/67375/H02-QW5Q88H5-V">Wiley Publishing Ltd</publisher><availability><licence>© 2015 Wiley Periodicals, Inc.</licence></availability><date type="published" when="2016-11"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Autophagy levels are elevated in barrett's esophagus and promote cell survival from acid and oxidative stress</title><title level="a" type="short">AUTOPHAGY ENHANCES BARRETT EPITHELIUM CELL SURVIVAL</title><author xml:id="author-0000"><persName><forename type="first">Jianping</forename><surname>Kong</surname></persName><affiliation><orgName type="division">Division of Gastroenterology</orgName><orgName type="institution">University of Pennsylvania</orgName><address><settlement>Philadelphia</settlement><region>Pennsylvania</region></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Kelly A.</forename><surname>Whelan</surname></persName><affiliation><orgName type="division">Division of Gastroenterology</orgName><orgName type="institution">University of Pennsylvania</orgName><address><settlement>Philadelphia</settlement><region>Pennsylvania</region></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Dorottya</forename><surname>Laczkó</surname></persName><affiliation><orgName type="division">Division of Gastroenterology</orgName><orgName type="institution">University of Pennsylvania</orgName><address><settlement>Philadelphia</settlement><region>Pennsylvania</region></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Brendan</forename><surname>Dang</surname></persName><affiliation><orgName type="division">Division of Gastroenterology</orgName><orgName type="institution">University of Pennsylvania</orgName><address><settlement>Philadelphia</settlement><region>Pennsylvania</region></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Angeliz</forename><surname>Caro Monroig</surname></persName><affiliation><orgName type="division">Division of Gastroenterology</orgName><orgName type="institution">University of Pennsylvania</orgName><address><settlement>Philadelphia</settlement><region>Pennsylvania</region></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Ali</forename><surname>Soroush</surname></persName><affiliation><orgName type="division">Division of Gastroenterology</orgName><orgName type="institution">University of Pennsylvania</orgName><address><settlement>Philadelphia</settlement><region>Pennsylvania</region></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">John</forename><surname>Falcone</surname></persName><affiliation><orgName type="division">Division of Gastroenterology</orgName><orgName type="institution">University of Pennsylvania</orgName><address><settlement>Philadelphia</settlement><region>Pennsylvania</region></address></affiliation></author><author xml:id="author-0007"><persName><forename type="first">Ravi K.</forename><surname>Amaravadi</surname></persName><affiliation><orgName type="division">Division of Hematology/Oncology</orgName><orgName type="institution">University of Pennsylvania</orgName><address><settlement>Philadelphia</settlement><region>Pennsylvania</region></address></affiliation><affiliation><orgName type="division">Department of Medicine, and the Abramson Cancer Center</orgName><orgName type="institution">University of Pennsylvania</orgName><address><settlement>Philadelphia</settlement><region>Pennsylvania</region></address></affiliation></author><author xml:id="author-0008"><persName><forename type="first">Anil K.</forename><surname>Rustgi</surname></persName><affiliation><orgName type="division">Division of Gastroenterology</orgName><orgName type="institution">University of Pennsylvania</orgName><address><settlement>Philadelphia</settlement><region>Pennsylvania</region></address></affiliation></author><author xml:id="author-0009"><persName><forename type="first">Gregory G.</forename><surname>Ginsberg</surname></persName><affiliation><orgName type="division">Division of Gastroenterology</orgName><orgName type="institution">University of Pennsylvania</orgName><address><settlement>Philadelphia</settlement><region>Pennsylvania</region></address></affiliation></author><author xml:id="author-0010"><persName><forename type="first">Gary W.</forename><surname>Falk</surname></persName><affiliation><orgName type="division">Division of Gastroenterology</orgName><orgName type="institution">University of Pennsylvania</orgName><address><settlement>Philadelphia</settlement><region>Pennsylvania</region></address></affiliation></author><author xml:id="author-0011"><persName><forename type="first">Hiroshi</forename><surname>Nakagawa</surname></persName><affiliation><orgName type="division">Division of Gastroenterology</orgName><orgName type="institution">University of Pennsylvania</orgName><address><settlement>Philadelphia</settlement><region>Pennsylvania</region></address></affiliation></author><author xml:id="author-0012" role="corresp"><persName><forename type="first">John P.</forename><surname>Lynch</surname></persName><email>lynchj@mail.med.upenn.edu</email><affiliation><orgName type="division">Division of Gastroenterology</orgName><orgName 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<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract xml:lang="en" style="main"><p>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.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="mc22406-kwd-0001">Barrett's esophagus</term><term xml:id="mc22406-kwd-0002">autophagy</term><term xml:id="mc22406-kwd-0003">oxidative stress</term><term xml:id="mc22406-kwd-0004">esophageal adenocarcinoma</term><term xml:id="mc22406-kwd-0005">chloroquine</term></keywords><keywords rend="articleCategory"><term>Article</term></keywords><keywords rend="tocHeading1"><term>Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-LTDG2T7K-C/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" xml:lang="en" type="serialArticle" xml:id="mc22406"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1002/(ISSN)1098-2744</doi><issn type="print">0899-1987</issn><issn type="electronic">1098-2744</issn><idGroup><id type="product" value="MC"></id></idGroup><titleGroup><title type="main" sort="MOLECULAR CARCINOGENESIS">Molecular Carcinogenesis</title><title type="short">Mol. 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number="10140"></count></countGroup><titleGroup><title type="main">Autophagy levels are elevated in barrett's esophagus and promote cell survival from acid and oxidative stress</title><title type="short">AUTOPHAGY ENHANCES BARRETT EPITHELIUM CELL SURVIVAL</title><title type="shortAuthors">KONG ET AL</title></titleGroup><creators><creator xml:id="mc22406-cr-0001" creatorRole="author" affiliationRef="#mc22406-aff-0001"><personName><givenNames>Jianping</givenNames> <familyName>Kong</familyName></personName></creator><creator xml:id="mc22406-cr-0002" creatorRole="author" affiliationRef="#mc22406-aff-0001"><personName><givenNames>Kelly A.</givenNames> <familyName>Whelan</familyName></personName></creator><creator xml:id="mc22406-cr-0003" creatorRole="author" affiliationRef="#mc22406-aff-0001"><personName><givenNames>Dorottya</givenNames> <familyName>Laczkó</familyName></personName></creator><creator xml:id="mc22406-cr-0004" creatorRole="author" 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xml:id="mc22406-kwd-0002">autophagy</keyword><keyword xml:id="mc22406-kwd-0003">oxidative stress</keyword><keyword xml:id="mc22406-kwd-0004">esophageal adenocarcinoma</keyword><keyword xml:id="mc22406-kwd-0005">chloroquine</keyword></keywordGroup><fundingInfo><fundingAgency fundRefName="National Cancer Institute" funderDoi="10.13039/100000054">NCI BETRNet program</fundingAgency><fundingNumber>CA163004 JPL</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Integrated Microphysiological Systems</fundingAgency><fundingNumber>TR 000536</fundingNumber></fundingInfo><fundingInfo><fundingAgency fundRefName="National Institutes of Health" funderDoi="10.13039/100000002">NIH</fundingAgency><fundingNumber>OD 012097</fundingNumber></fundingInfo><fundingInfo><fundingAgency>K26 RR 032714</fundingAgency></fundingInfo><fundingInfo><fundingAgency>University of Pennsylvania Transdisciplinary Research</fundingAgency></fundingInfo><fundingInfo><fundingAgency>K01DK103953</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Morphology, Cell Culture, and Molecular Biology Core Facilities of the Center</fundingAgency><fundingNumber>P30‐DK050306 PO1 CA098101</fundingNumber></fundingInfo><supportingInformation><p>Additional supporting information may be found in the online version of this article at the publisher's web‐site.</p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08991987:media:mc22406:mc22406-sup-0001-SupFig_Leg-S1"></mediaResource><caption>Supplemental Figure Legends.</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08991987:media:mc22406:mc22406-sup-0002-SupFig-S1"></mediaResource><caption><b>Figure S1</b>. Cyto‐ID fluorescence does not correlate with LC3‐GFP vesicle levels in OE19 cells.</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><section xml:id="mc22406-sec-0001"><p>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.</p></section></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="mc22406-note-0001" numbered="no">Jianping Kong and Kelly A. Whelan are co‐first authors.</note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Autophagy levels are elevated in barrett's esophagus and promote cell survival from acid and oxidative stress</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>AUTOPHAGY ENHANCES BARRETT EPITHELIUM CELL SURVIVAL</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Autophagy levels are elevated in barrett's esophagus and promote cell survival from acid and oxidative stress</title></titleInfo><name type="personal"><namePart type="given">Jianping</namePart><namePart type="family">Kong</namePart><affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kelly A.</namePart><namePart type="family">Whelan</namePart><affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dorottya</namePart><namePart type="family">Laczkó</namePart><affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Brendan</namePart><namePart type="family">Dang</namePart><affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Angeliz</namePart><namePart type="family">Caro Monroig</namePart><affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ali</namePart><namePart type="family">Soroush</namePart><affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John</namePart><namePart type="family">Falcone</namePart><affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ravi K.</namePart><namePart type="family">Amaravadi</namePart><affiliation>Division of Hematology/Oncology, University of Pennsylvania, Philadelphia, Pennsylvania</affiliation><affiliation>Department of Medicine, and the Abramson Cancer Center, University of Pennsylvania, Pennsylvania, Philadelphia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anil K.</namePart><namePart type="family">Rustgi</namePart><affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gregory G.</namePart><namePart type="family">Ginsberg</namePart><affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gary W.</namePart><namePart type="family">Falk</namePart><affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hiroshi</namePart><namePart type="family">Nakagawa</namePart><affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John P.</namePart><namePart type="family">Lynch</namePart><affiliation>Division of Gastroenterology, University of Pennsylvania, Pennsylvania, Philadelphia</affiliation><affiliation>E-mail: lynchj@mail.med.upenn.edu</affiliation><affiliation>Correspondence to: Division of Gastroenterology/912 BRB II/III, 421 Curie Blvd., Philadelphia, PA. 19104.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2016-11</dateIssued><dateCreated encoding="w3cdtf">2015-09-02</dateCreated><dateCaptured encoding="w3cdtf">2015-01-21</dateCaptured><dateValid encoding="w3cdtf">2015-08-17</dateValid><copyrightDate encoding="w3cdtf">2016</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">7</extent><extent unit="tables">0</extent><extent unit="words">10140</extent></physicalDescription><abstract 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.</abstract><note type="funding">NCI BETRNet program - No. CA163004 JPL; </note><note type="funding">Integrated Microphysiological Systems - No. TR 000536; </note><note type="funding">NIH - No. OD 012097; </note><note type="funding">K26 RR 032714</note><note type="funding">University of Pennsylvania Transdisciplinary Research</note><note type="funding">K01DK103953</note><note type="funding">Morphology, Cell Culture, and Molecular Biology Core Facilities of the Center - No. P30‐DK050306 PO1 CA098101; </note><subject lang="en"><genre>keywords</genre><topic>Barrett's esophagus</topic><topic>autophagy</topic><topic>oxidative stress</topic><topic>esophageal adenocarcinoma</topic><topic>chloroquine</topic></subject><relatedItem type="host"><titleInfo><title>Molecular Carcinogenesis</title></titleInfo><titleInfo type="abbreviated"><title>Mol. Carcinog.</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><note type="content"> Additional supporting information may be found in the online version of this article at the publisher's web‐site.Supporting Info Item: Supplemental Figure Legends. - Figure S1. Cyto‐ID fluorescence does not correlate with LC3‐GFP vesicle levels in OE19 cells. - </note><subject><genre>article-category</genre><topic>Article</topic><topic>Articles</topic></subject><identifier type="ISSN">0899-1987</identifier><identifier type="eISSN">1098-2744</identifier><identifier type="DOI">10.1002/(ISSN)1098-2744</identifier><identifier type="PublisherID">MC</identifier><part><date>2016</date><detail type="volume"><caption>vol.</caption><number>55</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>1526</start><end>1541</end><total>16</total></extent></part></relatedItem><relatedItem type="references" displayLabel="mc22406-cit-0001"><titleInfo><title>Society AC. Cancer facts and figures 2010. Atlanta, Ga: American Cancer Society; 2010.</title></titleInfo><note type="citation/reference">Society AC. Cancer facts and figures 2010. 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