ACE-2/ANG1-7 ameliorates ER stress-induced apoptosis in seawater aspiration-induced acute lung injury
Previous studies have shown that apoptosis of alveolar cells can be regulated by autocrine of angiotensin (ANG)II and its counter regulatory ACE-2/ANG1-7 axis. Our earlier study has shown that endoplasmic reticulum (ER) stress in response to seawater aspiration eventually led to apoptosis in lung ti...
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Veröffentlicht in: | American journal of physiology. Lung cellular and molecular physiology 2018-12, Vol.315 (6), p.L1015-L1027 |
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creator | Zhang, MinLong Gao, Yongheng Zhao, Weiguo Yu, Gaole Jin, Faguang |
description | Previous studies have shown that apoptosis of alveolar cells can be regulated by autocrine of angiotensin (ANG)II and its counter regulatory ACE-2/ANG1-7 axis. Our earlier study has shown that endoplasmic reticulum (ER) stress in response to seawater aspiration eventually led to apoptosis in lung tissue. In this study, we examined the hypothesis that ER stress-induced apoptosis in seawater aspiration-induced acute lung injury (ALI) might also be regulated by the ANGII/ANG1-7 system. ER stress was induced by seawater stimulation and proteasome inhibitor MG132 (an ER stress inductor). Moreover, ER stress in seawater-stimulated lung tissues and rat pulmonary microvascular endothelial cells (RPMVECs) promoted ANGII expression and decreased ACE-2/ANG1-7 expression. ER stress induced by seawater stimulation also led to apoptosis. Apoptosis induced by seawater stimulation and MG132 were inhibited by ANGII receptor blocker and abrogated by the addition of ANG1-7. These results suggest that apoptosis induced by ER stress in seawater aspiration-induced ALI is regulated by ANG II/ANG1-7 in lung tissues and RPMVECs. In addition, the active form of X-box binding protein 1 (XBP1), spliced XBP1 (XBP1s), a transcription factor that regulates ER-associated degradation genes during ER stress was significantly activated in seawater stimulated cells. Based on this phenomenon we designed a tandem gene, Wfs1 promoter (a target gene promoter of XBP1s)- ACE2 and ANG1-7 and transfected this tandem gene into seawater-stimulated cells. ACE-2/ANG1-7 expression were significantly promoted and apoptosis was inhibited in cells transfected with the tandem gene. These results suggest that stimulation of ACE-2/ANG1-7 may be a therapeutic target of ER stress-induced apoptosis in seawater aspiration-induced ALI. |
doi_str_mv | 10.1152/ajplung.00163.2018 |
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Our earlier study has shown that endoplasmic reticulum (ER) stress in response to seawater aspiration eventually led to apoptosis in lung tissue. In this study, we examined the hypothesis that ER stress-induced apoptosis in seawater aspiration-induced acute lung injury (ALI) might also be regulated by the ANGII/ANG1-7 system. ER stress was induced by seawater stimulation and proteasome inhibitor MG132 (an ER stress inductor). Moreover, ER stress in seawater-stimulated lung tissues and rat pulmonary microvascular endothelial cells (RPMVECs) promoted ANGII expression and decreased ACE-2/ANG1-7 expression. ER stress induced by seawater stimulation also led to apoptosis. Apoptosis induced by seawater stimulation and MG132 were inhibited by ANGII receptor blocker and abrogated by the addition of ANG1-7. These results suggest that apoptosis induced by ER stress in seawater aspiration-induced ALI is regulated by ANG II/ANG1-7 in lung tissues and RPMVECs. In addition, the active form of X-box binding protein 1 (XBP1), spliced XBP1 (XBP1s), a transcription factor that regulates ER-associated degradation genes during ER stress was significantly activated in seawater stimulated cells. Based on this phenomenon we designed a tandem gene, Wfs1 promoter (a target gene promoter of XBP1s)- ACE2 and ANG1-7 and transfected this tandem gene into seawater-stimulated cells. ACE-2/ANG1-7 expression were significantly promoted and apoptosis was inhibited in cells transfected with the tandem gene. These results suggest that stimulation of ACE-2/ANG1-7 may be a therapeutic target of ER stress-induced apoptosis in seawater aspiration-induced ALI.</description><identifier>ISSN: 1040-0605</identifier><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 1522-1504</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajplung.00163.2018</identifier><identifier>PMID: 30335496</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>ACE2 ; Activating transcription factor 1 ; Alveoli ; Angiotensin ; Angiotensin II ; Angiotensin-converting enzyme 2 ; Apoptosis ; Autocrine signalling ; Endoplasmic reticulum ; Endothelial cells ; Lung diseases ; Microvasculature ; Proteasome inhibitors ; Seawater ; Therapeutic applications</subject><ispartof>American journal of physiology. Lung cellular and molecular physiology, 2018-12, Vol.315 (6), p.L1015-L1027</ispartof><rights>Copyright American Physiological Society Dec 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c441t-82932d512c02457bf635ae34816cb7e945dadaf21784142e8073cca7c6982f0f3</citedby><cites>FETCH-LOGICAL-c441t-82932d512c02457bf635ae34816cb7e945dadaf21784142e8073cca7c6982f0f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30335496$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, MinLong</creatorcontrib><creatorcontrib>Gao, Yongheng</creatorcontrib><creatorcontrib>Zhao, Weiguo</creatorcontrib><creatorcontrib>Yu, Gaole</creatorcontrib><creatorcontrib>Jin, Faguang</creatorcontrib><title>ACE-2/ANG1-7 ameliorates ER stress-induced apoptosis in seawater aspiration-induced acute lung injury</title><title>American journal of physiology. Lung cellular and molecular physiology</title><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><description>Previous studies have shown that apoptosis of alveolar cells can be regulated by autocrine of angiotensin (ANG)II and its counter regulatory ACE-2/ANG1-7 axis. Our earlier study has shown that endoplasmic reticulum (ER) stress in response to seawater aspiration eventually led to apoptosis in lung tissue. In this study, we examined the hypothesis that ER stress-induced apoptosis in seawater aspiration-induced acute lung injury (ALI) might also be regulated by the ANGII/ANG1-7 system. ER stress was induced by seawater stimulation and proteasome inhibitor MG132 (an ER stress inductor). Moreover, ER stress in seawater-stimulated lung tissues and rat pulmonary microvascular endothelial cells (RPMVECs) promoted ANGII expression and decreased ACE-2/ANG1-7 expression. ER stress induced by seawater stimulation also led to apoptosis. Apoptosis induced by seawater stimulation and MG132 were inhibited by ANGII receptor blocker and abrogated by the addition of ANG1-7. These results suggest that apoptosis induced by ER stress in seawater aspiration-induced ALI is regulated by ANG II/ANG1-7 in lung tissues and RPMVECs. In addition, the active form of X-box binding protein 1 (XBP1), spliced XBP1 (XBP1s), a transcription factor that regulates ER-associated degradation genes during ER stress was significantly activated in seawater stimulated cells. Based on this phenomenon we designed a tandem gene, Wfs1 promoter (a target gene promoter of XBP1s)- ACE2 and ANG1-7 and transfected this tandem gene into seawater-stimulated cells. ACE-2/ANG1-7 expression were significantly promoted and apoptosis was inhibited in cells transfected with the tandem gene. These results suggest that stimulation of ACE-2/ANG1-7 may be a therapeutic target of ER stress-induced apoptosis in seawater aspiration-induced ALI.</description><subject>ACE2</subject><subject>Activating transcription factor 1</subject><subject>Alveoli</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin-converting enzyme 2</subject><subject>Apoptosis</subject><subject>Autocrine signalling</subject><subject>Endoplasmic reticulum</subject><subject>Endothelial cells</subject><subject>Lung diseases</subject><subject>Microvasculature</subject><subject>Proteasome inhibitors</subject><subject>Seawater</subject><subject>Therapeutic applications</subject><issn>1040-0605</issn><issn>1931-857X</issn><issn>1522-1504</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNpdkU1Lw0AQhhdRbK3-AQ8S8OIl7ezsR9JjKbUKRUH0HLabjWzIl7sJ0n_v1lYFTzMwzzvzMi8h1xSmlAqcqbKrhuZ9CkAlmyLQ9ISMwwBjKoCfhh44xCBBjMiF9yUACAB5TkYMGBN8LsfELJarGGeLpzWNk0jVprKtU73x0eol8r0z3se2yQdt8kh1bde33vrINpE36jNwLlK-s0Fh2-YP1ENvor23QJaD212Ss0JV3lwd64S83a9elw_x5nn9uFxsYs057eMU5wxzQVEDcpFsC8mEMoynVOptYuZc5CpXBdIk5ZSjSSFhWqtEy3mKBRRsQu4OezvXfgzG91ltvTZVpRrTDj5DiizBFBkN6O0_tGwH1wR3gZLhvEyQBwoPlHat984UWedsrdwuo5DtQ8iOIWTfIWT7EILo5rh62NYm_5X8fJ19AY5zgqA</recordid><startdate>20181201</startdate><enddate>20181201</enddate><creator>Zhang, MinLong</creator><creator>Gao, Yongheng</creator><creator>Zhao, Weiguo</creator><creator>Yu, Gaole</creator><creator>Jin, Faguang</creator><general>American Physiological Society</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20181201</creationdate><title>ACE-2/ANG1-7 ameliorates ER stress-induced apoptosis in seawater aspiration-induced acute lung injury</title><author>Zhang, MinLong ; Gao, Yongheng ; Zhao, Weiguo ; Yu, Gaole ; Jin, Faguang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c441t-82932d512c02457bf635ae34816cb7e945dadaf21784142e8073cca7c6982f0f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>ACE2</topic><topic>Activating transcription factor 1</topic><topic>Alveoli</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin-converting enzyme 2</topic><topic>Apoptosis</topic><topic>Autocrine signalling</topic><topic>Endoplasmic reticulum</topic><topic>Endothelial cells</topic><topic>Lung diseases</topic><topic>Microvasculature</topic><topic>Proteasome inhibitors</topic><topic>Seawater</topic><topic>Therapeutic applications</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, MinLong</creatorcontrib><creatorcontrib>Gao, Yongheng</creatorcontrib><creatorcontrib>Zhao, Weiguo</creatorcontrib><creatorcontrib>Yu, Gaole</creatorcontrib><creatorcontrib>Jin, Faguang</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology. Lung cellular and molecular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, MinLong</au><au>Gao, Yongheng</au><au>Zhao, Weiguo</au><au>Yu, Gaole</au><au>Jin, Faguang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ACE-2/ANG1-7 ameliorates ER stress-induced apoptosis in seawater aspiration-induced acute lung injury</atitle><jtitle>American journal of physiology. Lung cellular and molecular physiology</jtitle><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><date>2018-12-01</date><risdate>2018</risdate><volume>315</volume><issue>6</issue><spage>L1015</spage><epage>L1027</epage><pages>L1015-L1027</pages><issn>1040-0605</issn><issn>1931-857X</issn><eissn>1522-1504</eissn><eissn>1522-1466</eissn><abstract>Previous studies have shown that apoptosis of alveolar cells can be regulated by autocrine of angiotensin (ANG)II and its counter regulatory ACE-2/ANG1-7 axis. Our earlier study has shown that endoplasmic reticulum (ER) stress in response to seawater aspiration eventually led to apoptosis in lung tissue. In this study, we examined the hypothesis that ER stress-induced apoptosis in seawater aspiration-induced acute lung injury (ALI) might also be regulated by the ANGII/ANG1-7 system. ER stress was induced by seawater stimulation and proteasome inhibitor MG132 (an ER stress inductor). Moreover, ER stress in seawater-stimulated lung tissues and rat pulmonary microvascular endothelial cells (RPMVECs) promoted ANGII expression and decreased ACE-2/ANG1-7 expression. ER stress induced by seawater stimulation also led to apoptosis. Apoptosis induced by seawater stimulation and MG132 were inhibited by ANGII receptor blocker and abrogated by the addition of ANG1-7. These results suggest that apoptosis induced by ER stress in seawater aspiration-induced ALI is regulated by ANG II/ANG1-7 in lung tissues and RPMVECs. In addition, the active form of X-box binding protein 1 (XBP1), spliced XBP1 (XBP1s), a transcription factor that regulates ER-associated degradation genes during ER stress was significantly activated in seawater stimulated cells. Based on this phenomenon we designed a tandem gene, Wfs1 promoter (a target gene promoter of XBP1s)- ACE2 and ANG1-7 and transfected this tandem gene into seawater-stimulated cells. ACE-2/ANG1-7 expression were significantly promoted and apoptosis was inhibited in cells transfected with the tandem gene. These results suggest that stimulation of ACE-2/ANG1-7 may be a therapeutic target of ER stress-induced apoptosis in seawater aspiration-induced ALI.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>30335496</pmid><doi>10.1152/ajplung.00163.2018</doi><oa>free_for_read</oa></addata></record> |
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subjects | ACE2 Activating transcription factor 1 Alveoli Angiotensin Angiotensin II Angiotensin-converting enzyme 2 Apoptosis Autocrine signalling Endoplasmic reticulum Endothelial cells Lung diseases Microvasculature Proteasome inhibitors Seawater Therapeutic applications |
title | ACE-2/ANG1-7 ameliorates ER stress-induced apoptosis in seawater aspiration-induced acute lung injury |
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