β1-Na+,K+-ATPase gene therapy upregulates tight junctions to rescue lipopolysaccharide-induced acute lung injury
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are associated with diverse disorders and characterized by disruption of the alveolar-capillary barrier, leakage of edema fluid into the lung, and substantial inflammation leading to acute respiratory failure. Gene therapy is a p...
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| Veröffentlicht in: | Gene therapy 2016-06, Vol.23 (6), p.489-499 |
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| creator | Lin, X Barravecchia, M Kothari, P Young, J L Dean, D A |
| description | Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are associated with diverse disorders and characterized by disruption of the alveolar-capillary barrier, leakage of edema fluid into the lung, and substantial inflammation leading to acute respiratory failure. Gene therapy is a potentially powerful approach to treat ALI/ARDS through repair of alveolar epithelial function. Herein, we show that delivery of a plasmid expressing β1-subunit of the Na
+
,K
+
-ATPase (β1-Na
+
,K
+
-ATPase) alone or in combination with epithelial sodium channel (ENaC) α1-subunit using electroporation not only protected from subsequent lipopolysaccharide (LPS)-mediated lung injury, but also treated injured lungs. However, transfer of α1-subunit of ENaC (α1-ENaC) alone only provided protection benefit rather than treatment benefit although alveolar fluid clearance had been remarkably enhanced. Gene transfer of β1-Na
+
,K
+
-ATPase, but not α1-ENaC, not only enhanced expression of tight junction protein zona occludins-1 (ZO-1) and occludin both in cultured cells and in mouse lungs, but also reduced pre-existing increase of lung permeability
in vivo
. These results demonstrate that gene transfer of β1-Na
+
,K
+
-ATPase upregulates tight junction formation and therefore treats lungs with existing injury, whereas delivery of α1-ENaC only maintains pre-existing tight junction but not for generation. This indicates that the restoration of epithelial/endothelial barrier function may provide better treatment of ALI/ARDS. |
| doi_str_mv | 10.1038/gt.2016.19 |
| format | Article |
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+
,K
+
-ATPase (β1-Na
+
,K
+
-ATPase) alone or in combination with epithelial sodium channel (ENaC) α1-subunit using electroporation not only protected from subsequent lipopolysaccharide (LPS)-mediated lung injury, but also treated injured lungs. However, transfer of α1-subunit of ENaC (α1-ENaC) alone only provided protection benefit rather than treatment benefit although alveolar fluid clearance had been remarkably enhanced. Gene transfer of β1-Na
+
,K
+
-ATPase, but not α1-ENaC, not only enhanced expression of tight junction protein zona occludins-1 (ZO-1) and occludin both in cultured cells and in mouse lungs, but also reduced pre-existing increase of lung permeability
in vivo
. These results demonstrate that gene transfer of β1-Na
+
,K
+
-ATPase upregulates tight junction formation and therefore treats lungs with existing injury, whereas delivery of α1-ENaC only maintains pre-existing tight junction but not for generation. This indicates that the restoration of epithelial/endothelial barrier function may provide better treatment of ALI/ARDS.</description><identifier>ISSN: 0969-7128</identifier><identifier>EISSN: 1476-5462</identifier><identifier>DOI: 10.1038/gt.2016.19</identifier><identifier>PMID: 26910760</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>42 ; 631/61/2300 ; 631/61/2300/1851 ; 631/61/51/201 ; 631/80 ; 631/80/79/1987 ; 64 ; 64/60 ; 692/699/1785 ; 96/109 ; Acute Lung Injury - chemically induced ; Acute Lung Injury - enzymology ; Acute Lung Injury - genetics ; Acute Lung Injury - therapy ; Alveoli ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Disease Models, Animal ; Edema ; Electroporation ; Electroporation - methods ; Epithelial Sodium Channels - therapeutic use ; Gene Expression ; Gene Therapy ; Genetic Therapy - methods ; Human Genetics ; Lipopolysaccharides ; Lungs ; Male ; Mice ; Mice, Inbred C57BL ; Na+/K+-exchanging ATPase ; Nanotechnology ; original-article ; Permeability ; Plasmids - administration & dosage ; Plasmids - genetics ; Respiratory distress syndrome ; Respiratory Distress Syndrome, Adult - therapy ; Respiratory failure ; Sodium-Potassium-Exchanging ATPase - administration & dosage ; Sodium-Potassium-Exchanging ATPase - genetics ; Tight junctions ; Tight Junctions - enzymology ; Tight Junctions - genetics ; Tight Junctions - metabolism ; Up-Regulation ; Zonula occludens-1 protein</subject><ispartof>Gene therapy, 2016-06, Vol.23 (6), p.489-499</ispartof><rights>Macmillan Publishers Limited 2016</rights><rights>Macmillan Publishers Limited 2016.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3029-f47938e093651462f4ce24c09b7dc37cc9d9278699bcd98e0e389e4e22f6026d3</citedby><cites>FETCH-LOGICAL-c3029-f47938e093651462f4ce24c09b7dc37cc9d9278699bcd98e0e389e4e22f6026d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/gt.2016.19$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/gt.2016.19$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26910760$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, X</creatorcontrib><creatorcontrib>Barravecchia, M</creatorcontrib><creatorcontrib>Kothari, P</creatorcontrib><creatorcontrib>Young, J L</creatorcontrib><creatorcontrib>Dean, D A</creatorcontrib><title>β1-Na+,K+-ATPase gene therapy upregulates tight junctions to rescue lipopolysaccharide-induced acute lung injury</title><title>Gene therapy</title><addtitle>Gene Ther</addtitle><addtitle>Gene Ther</addtitle><description>Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are associated with diverse disorders and characterized by disruption of the alveolar-capillary barrier, leakage of edema fluid into the lung, and substantial inflammation leading to acute respiratory failure. Gene therapy is a potentially powerful approach to treat ALI/ARDS through repair of alveolar epithelial function. Herein, we show that delivery of a plasmid expressing β1-subunit of the Na
+
,K
+
-ATPase (β1-Na
+
,K
+
-ATPase) alone or in combination with epithelial sodium channel (ENaC) α1-subunit using electroporation not only protected from subsequent lipopolysaccharide (LPS)-mediated lung injury, but also treated injured lungs. However, transfer of α1-subunit of ENaC (α1-ENaC) alone only provided protection benefit rather than treatment benefit although alveolar fluid clearance had been remarkably enhanced. Gene transfer of β1-Na
+
,K
+
-ATPase, but not α1-ENaC, not only enhanced expression of tight junction protein zona occludins-1 (ZO-1) and occludin both in cultured cells and in mouse lungs, but also reduced pre-existing increase of lung permeability
in vivo
. These results demonstrate that gene transfer of β1-Na
+
,K
+
-ATPase upregulates tight junction formation and therefore treats lungs with existing injury, whereas delivery of α1-ENaC only maintains pre-existing tight junction but not for generation. This indicates that the restoration of epithelial/endothelial barrier function may provide better treatment of ALI/ARDS.</description><subject>42</subject><subject>631/61/2300</subject><subject>631/61/2300/1851</subject><subject>631/61/51/201</subject><subject>631/80</subject><subject>631/80/79/1987</subject><subject>64</subject><subject>64/60</subject><subject>692/699/1785</subject><subject>96/109</subject><subject>Acute Lung Injury - chemically induced</subject><subject>Acute Lung Injury - enzymology</subject><subject>Acute Lung Injury - genetics</subject><subject>Acute Lung Injury - therapy</subject><subject>Alveoli</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Disease Models, Animal</subject><subject>Edema</subject><subject>Electroporation</subject><subject>Electroporation - methods</subject><subject>Epithelial Sodium Channels - therapeutic use</subject><subject>Gene Expression</subject><subject>Gene Therapy</subject><subject>Genetic Therapy - methods</subject><subject>Human Genetics</subject><subject>Lipopolysaccharides</subject><subject>Lungs</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Na+/K+-exchanging ATPase</subject><subject>Nanotechnology</subject><subject>original-article</subject><subject>Permeability</subject><subject>Plasmids - administration & dosage</subject><subject>Plasmids - genetics</subject><subject>Respiratory distress syndrome</subject><subject>Respiratory Distress Syndrome, Adult - therapy</subject><subject>Respiratory failure</subject><subject>Sodium-Potassium-Exchanging ATPase - administration & dosage</subject><subject>Sodium-Potassium-Exchanging ATPase - genetics</subject><subject>Tight junctions</subject><subject>Tight Junctions - enzymology</subject><subject>Tight Junctions - genetics</subject><subject>Tight Junctions - metabolism</subject><subject>Up-Regulation</subject><subject>Zonula occludens-1 protein</subject><issn>0969-7128</issn><issn>1476-5462</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpt0ctOGzEUBmCrKioBuukDVJa6QaQTbI-xx8sIQYuIWhZhbTmeM5OJJp7Bl0VeiwfpM-EotJUQK8vyp_9cjNAXSmaUlNVlG2eMUDGj6gOaUC5FccUF-4gmRAlVSMqqY3QSwoYQwmXFPqFjJhQlUpAJevrzTItfZvr9flrMlw8mAG7BAY5r8Gbc4TR6aFNvIgQcu3Yd8SY5G7vB5fuAPQSbAPfdOIxDvwvG2rXxXQ1F5-pkocbGpphBci3u3Cb53Rk6akwf4PPreYoeb2-W1z-Lxe8fd9fzRWFLwlTRcKnKCogqxRXN4zTcAuOWqJWsbSmtVbVishJKrWytMoSyUsCBsUYQJuryFJ0fckc_PCUIUW-7YKHvjYMhBU1zvtrvT2b67Q3dDMm73J1mgnMhKiJoVhcHZf0QgodGj77bGr_TlOh9kG6j3n-Epirjr6-RabWF-h_9u_kMpgcQ8pNrwf-v-U7cC2Gzkdw</recordid><startdate>20160601</startdate><enddate>20160601</enddate><creator>Lin, X</creator><creator>Barravecchia, M</creator><creator>Kothari, P</creator><creator>Young, J L</creator><creator>Dean, D A</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20160601</creationdate><title>β1-Na+,K+-ATPase gene therapy upregulates tight junctions to rescue lipopolysaccharide-induced acute lung injury</title><author>Lin, X ; Barravecchia, M ; Kothari, P ; Young, J L ; Dean, D A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3029-f47938e093651462f4ce24c09b7dc37cc9d9278699bcd98e0e389e4e22f6026d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>42</topic><topic>631/61/2300</topic><topic>631/61/2300/1851</topic><topic>631/61/51/201</topic><topic>631/80</topic><topic>631/80/79/1987</topic><topic>64</topic><topic>64/60</topic><topic>692/699/1785</topic><topic>96/109</topic><topic>Acute Lung Injury - chemically induced</topic><topic>Acute Lung Injury - enzymology</topic><topic>Acute Lung Injury - genetics</topic><topic>Acute Lung Injury - therapy</topic><topic>Alveoli</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Disease Models, Animal</topic><topic>Edema</topic><topic>Electroporation</topic><topic>Electroporation - methods</topic><topic>Epithelial Sodium Channels - therapeutic use</topic><topic>Gene Expression</topic><topic>Gene Therapy</topic><topic>Genetic Therapy - methods</topic><topic>Human Genetics</topic><topic>Lipopolysaccharides</topic><topic>Lungs</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Na+/K+-exchanging ATPase</topic><topic>Nanotechnology</topic><topic>original-article</topic><topic>Permeability</topic><topic>Plasmids - administration & dosage</topic><topic>Plasmids - genetics</topic><topic>Respiratory distress syndrome</topic><topic>Respiratory Distress Syndrome, Adult - therapy</topic><topic>Respiratory failure</topic><topic>Sodium-Potassium-Exchanging ATPase - administration & dosage</topic><topic>Sodium-Potassium-Exchanging ATPase - genetics</topic><topic>Tight junctions</topic><topic>Tight Junctions - enzymology</topic><topic>Tight Junctions - genetics</topic><topic>Tight Junctions - metabolism</topic><topic>Up-Regulation</topic><topic>Zonula occludens-1 protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, X</creatorcontrib><creatorcontrib>Barravecchia, M</creatorcontrib><creatorcontrib>Kothari, P</creatorcontrib><creatorcontrib>Young, J L</creatorcontrib><creatorcontrib>Dean, D A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Gene therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, X</au><au>Barravecchia, M</au><au>Kothari, P</au><au>Young, J L</au><au>Dean, D A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>β1-Na+,K+-ATPase gene therapy upregulates tight junctions to rescue lipopolysaccharide-induced acute lung injury</atitle><jtitle>Gene therapy</jtitle><stitle>Gene Ther</stitle><addtitle>Gene Ther</addtitle><date>2016-06-01</date><risdate>2016</risdate><volume>23</volume><issue>6</issue><spage>489</spage><epage>499</epage><pages>489-499</pages><issn>0969-7128</issn><eissn>1476-5462</eissn><abstract>Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are associated with diverse disorders and characterized by disruption of the alveolar-capillary barrier, leakage of edema fluid into the lung, and substantial inflammation leading to acute respiratory failure. Gene therapy is a potentially powerful approach to treat ALI/ARDS through repair of alveolar epithelial function. Herein, we show that delivery of a plasmid expressing β1-subunit of the Na
+
,K
+
-ATPase (β1-Na
+
,K
+
-ATPase) alone or in combination with epithelial sodium channel (ENaC) α1-subunit using electroporation not only protected from subsequent lipopolysaccharide (LPS)-mediated lung injury, but also treated injured lungs. However, transfer of α1-subunit of ENaC (α1-ENaC) alone only provided protection benefit rather than treatment benefit although alveolar fluid clearance had been remarkably enhanced. Gene transfer of β1-Na
+
,K
+
-ATPase, but not α1-ENaC, not only enhanced expression of tight junction protein zona occludins-1 (ZO-1) and occludin both in cultured cells and in mouse lungs, but also reduced pre-existing increase of lung permeability
in vivo
. These results demonstrate that gene transfer of β1-Na
+
,K
+
-ATPase upregulates tight junction formation and therefore treats lungs with existing injury, whereas delivery of α1-ENaC only maintains pre-existing tight junction but not for generation. This indicates that the restoration of epithelial/endothelial barrier function may provide better treatment of ALI/ARDS.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>26910760</pmid><doi>10.1038/gt.2016.19</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Gene therapy, 2016-06, Vol.23 (6), p.489-499 |
| issn | 0969-7128 1476-5462 |
| language | eng |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | 42 631/61/2300 631/61/2300/1851 631/61/51/201 631/80 631/80/79/1987 64 64/60 692/699/1785 96/109 Acute Lung Injury - chemically induced Acute Lung Injury - enzymology Acute Lung Injury - genetics Acute Lung Injury - therapy Alveoli Animals Biomedical and Life Sciences Biomedicine Cell Biology Disease Models, Animal Edema Electroporation Electroporation - methods Epithelial Sodium Channels - therapeutic use Gene Expression Gene Therapy Genetic Therapy - methods Human Genetics Lipopolysaccharides Lungs Male Mice Mice, Inbred C57BL Na+/K+-exchanging ATPase Nanotechnology original-article Permeability Plasmids - administration & dosage Plasmids - genetics Respiratory distress syndrome Respiratory Distress Syndrome, Adult - therapy Respiratory failure Sodium-Potassium-Exchanging ATPase - administration & dosage Sodium-Potassium-Exchanging ATPase - genetics Tight junctions Tight Junctions - enzymology Tight Junctions - genetics Tight Junctions - metabolism Up-Regulation Zonula occludens-1 protein |
| title | β1-Na+,K+-ATPase gene therapy upregulates tight junctions to rescue lipopolysaccharide-induced acute lung injury |
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