Identification of distinct genes associated with seawater aspiration-induced acute lung injury by gene expression profile analysis
Seawater aspiration-induced acute lung injury (ALI) is a syndrome associated with a high mortality rate, which is characterized by severe hypoxemia, pulmonary edema and inflammation. The present study is the first, to the best of our knowledge, to analyze gene expression profiles from a rat model of...
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description | Seawater aspiration-induced acute lung injury (ALI) is a syndrome associated with a high mortality rate, which is characterized by severe hypoxemia, pulmonary edema and inflammation. The present study is the first, to the best of our knowledge, to analyze gene expression profiles from a rat model of seawater aspiration-induced ALI. Adult male Sprague-Dawley rats were instilled with seawater (4 ml/kg) in the seawater aspiration-induced ALI group (S group) or with distilled water (4 ml/kg) in the distilled water negative control group (D group). In the blank control group (C group) the rats' tracheae were exposed without instillation. Subsequently, lung samples were examined by histopathology; total protein concentration was detected in bronchoalveolar lavage fluid (BALF); lung wet/dry weight ratios were determined; and transcript expression was detected by gene sequencing analysis. The results demonstrated that histopathological alterations, pulmonary edema and total protein concentrations in BALF were increased in the S group compared with in the D group. Analysis of differential gene expression identified up and downregulated genes in the S group compared with in the D and C groups. A gene ontology analysis of the differential gene expression revealed enrichment of genes in the functional pathways associated with neutrophil chemotaxis, immune and defense responses, and cytokine activity. Kyoto Encyclopedia of Genes and Genomes analysis revealed that the cytokine-cytokine receptor interaction pathway was one of the most important pathways involved in seawater aspiration-induced ALI. In conclusion, activation of the cytokine-cytokine receptor interaction pathway may have an essential role in the progression of seawater aspiration-induced ALI, and the downregulation of tumor necrosis factor superfamily member 10 may enhance inflammation. Furthermore, IL-6 may be considered a biomarker in seawater aspiration-induced ALI. |
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The present study is the first, to the best of our knowledge, to analyze gene expression profiles from a rat model of seawater aspiration-induced ALI. Adult male Sprague-Dawley rats were instilled with seawater (4 ml/kg) in the seawater aspiration-induced ALI group (S group) or with distilled water (4 ml/kg) in the distilled water negative control group (D group). In the blank control group (C group) the rats' tracheae were exposed without instillation. Subsequently, lung samples were examined by histopathology; total protein concentration was detected in bronchoalveolar lavage fluid (BALF); lung wet/dry weight ratios were determined; and transcript expression was detected by gene sequencing analysis. The results demonstrated that histopathological alterations, pulmonary edema and total protein concentrations in BALF were increased in the S group compared with in the D group. Analysis of differential gene expression identified up and downregulated genes in the S group compared with in the D and C groups. A gene ontology analysis of the differential gene expression revealed enrichment of genes in the functional pathways associated with neutrophil chemotaxis, immune and defense responses, and cytokine activity. Kyoto Encyclopedia of Genes and Genomes analysis revealed that the cytokine-cytokine receptor interaction pathway was one of the most important pathways involved in seawater aspiration-induced ALI. In conclusion, activation of the cytokine-cytokine receptor interaction pathway may have an essential role in the progression of seawater aspiration-induced ALI, and the downregulation of tumor necrosis factor superfamily member 10 may enhance inflammation. Furthermore, IL-6 may be considered a biomarker in seawater aspiration-induced ALI.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2016.5607</identifier><identifier>PMID: 27509884</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Acute Lung Injury - genetics ; Acute Lung Injury - pathology ; Acute respiratory distress syndrome ; Alveoli ; Animals ; Bronchoalveolar Lavage Fluid ; Bronchus ; Care and treatment ; Chemokines ; Chemotaxis ; Cytokines ; Development and progression ; Disease Models, Animal ; Edema ; Gene expression ; gene expression profiles ; Gene Expression Regulation ; Gene Ontology ; Genetic aspects ; Genomes ; Genotype ; Health aspects ; Histopathology ; Hypoxemia ; IL-6 ; Interleukin 6 ; Kinases ; Laboratory animals ; Lung - metabolism ; Lung - pathology ; Lungs ; Male ; Neutrophils ; Rats, Sprague-Dawley ; Rodents ; Seawater - adverse effects ; seawater aspiration-induced ALI ; Sepsis ; TNFSF10 ; Transcription ; Transcriptome</subject><ispartof>Molecular medicine reports, 2016-10, Vol.14 (4), p.3168-3178</ispartof><rights>Copyright: © Liu et al.</rights><rights>COPYRIGHT 2016 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2016</rights><rights>Copyright: © Liu et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-482ac02ee4c567ca13d91697aea7ba2e91a9767c3891ff8d6bfab238496a36ac3</citedby><cites>FETCH-LOGICAL-c514t-482ac02ee4c567ca13d91697aea7ba2e91a9767c3891ff8d6bfab238496a36ac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27509884$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Wei</creatorcontrib><creatorcontrib>Pan, Lei</creatorcontrib><creatorcontrib>Zhang, Minlong</creatorcontrib><creatorcontrib>Bo, Liyan</creatorcontrib><creatorcontrib>Li, Congcong</creatorcontrib><creatorcontrib>Liu, Qingqing</creatorcontrib><creatorcontrib>Wang, Li</creatorcontrib><creatorcontrib>Jin, Faguang</creatorcontrib><title>Identification of distinct genes associated with seawater aspiration-induced acute lung injury by gene expression profile analysis</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Seawater aspiration-induced acute lung injury (ALI) is a syndrome associated with a high mortality rate, which is characterized by severe hypoxemia, pulmonary edema and inflammation. The present study is the first, to the best of our knowledge, to analyze gene expression profiles from a rat model of seawater aspiration-induced ALI. Adult male Sprague-Dawley rats were instilled with seawater (4 ml/kg) in the seawater aspiration-induced ALI group (S group) or with distilled water (4 ml/kg) in the distilled water negative control group (D group). In the blank control group (C group) the rats' tracheae were exposed without instillation. Subsequently, lung samples were examined by histopathology; total protein concentration was detected in bronchoalveolar lavage fluid (BALF); lung wet/dry weight ratios were determined; and transcript expression was detected by gene sequencing analysis. The results demonstrated that histopathological alterations, pulmonary edema and total protein concentrations in BALF were increased in the S group compared with in the D group. Analysis of differential gene expression identified up and downregulated genes in the S group compared with in the D and C groups. A gene ontology analysis of the differential gene expression revealed enrichment of genes in the functional pathways associated with neutrophil chemotaxis, immune and defense responses, and cytokine activity. Kyoto Encyclopedia of Genes and Genomes analysis revealed that the cytokine-cytokine receptor interaction pathway was one of the most important pathways involved in seawater aspiration-induced ALI. In conclusion, activation of the cytokine-cytokine receptor interaction pathway may have an essential role in the progression of seawater aspiration-induced ALI, and the downregulation of tumor necrosis factor superfamily member 10 may enhance inflammation. Furthermore, IL-6 may be considered a biomarker in seawater aspiration-induced ALI.</description><subject>Acute Lung Injury - genetics</subject><subject>Acute Lung Injury - pathology</subject><subject>Acute respiratory distress syndrome</subject><subject>Alveoli</subject><subject>Animals</subject><subject>Bronchoalveolar Lavage Fluid</subject><subject>Bronchus</subject><subject>Care and treatment</subject><subject>Chemokines</subject><subject>Chemotaxis</subject><subject>Cytokines</subject><subject>Development and progression</subject><subject>Disease Models, Animal</subject><subject>Edema</subject><subject>Gene expression</subject><subject>gene expression profiles</subject><subject>Gene Expression Regulation</subject><subject>Gene Ontology</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Genotype</subject><subject>Health aspects</subject><subject>Histopathology</subject><subject>Hypoxemia</subject><subject>IL-6</subject><subject>Interleukin 6</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Lungs</subject><subject>Male</subject><subject>Neutrophils</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Seawater - adverse effects</subject><subject>seawater aspiration-induced ALI</subject><subject>Sepsis</subject><subject>TNFSF10</subject><subject>Transcription</subject><subject>Transcriptome</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkkFv1DAQhSMEoqVw5IoscYBLFttxnPiCVFVQKlXiAmdr1p5svUrsYCcte-WX43S3C0XIB9uab97ojV5RvGZ0VbWKfxiGuOKUyVUtafOkOGWNYmVFqXh6eHOlmpPiRUpbSmXNa_W8OOFNTVXbitPi15VFP7nOGZhc8CR0xLo0OW8mskGPiUBKwTiY0JI7N92QhHCXfzEXRhfvu0rn7WwyAGaekPSz3xDnt3PckfXuXobgzzFiSsuIMYbO9UjAQ79LLr0snnXQJ3x1uM-K758_fbv4Ul5_vby6OL8uTc3EVIqWg6EcUZhaNgZYZRWTqgGEZg0cFQPV5ELeCuu61sp1B2tetUJJqCSY6qz4uNcd5_WA1mTfEXo9RjdA3OkATj-ueHejN-FW11TwvMks8P4gEMOPGdOkB5cM9j14DHPSrOW0VqoSbUbf_oNuwxyz4UypiotGZcU_1AZ61M53Ic81i6g-FzKbUZKKTK3-Q-VjcXAmeFy2-bih3DeYGFKK2B09MqqX0OgcGr2ERi-hyfybvxdzpB9SkoF3eyCN4K2zIR2ZrFQyUVJRVky21W8Pxc1V</recordid><startdate>20161001</startdate><enddate>20161001</enddate><creator>Liu, Wei</creator><creator>Pan, Lei</creator><creator>Zhang, Minlong</creator><creator>Bo, Liyan</creator><creator>Li, Congcong</creator><creator>Liu, Qingqing</creator><creator>Wang, Li</creator><creator>Jin, Faguang</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20161001</creationdate><title>Identification of distinct genes associated with seawater aspiration-induced acute lung injury by gene expression profile analysis</title><author>Liu, Wei ; Pan, Lei ; Zhang, Minlong ; Bo, Liyan ; Li, Congcong ; Liu, Qingqing ; Wang, Li ; Jin, Faguang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-482ac02ee4c567ca13d91697aea7ba2e91a9767c3891ff8d6bfab238496a36ac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Acute Lung Injury - genetics</topic><topic>Acute Lung Injury - pathology</topic><topic>Acute respiratory distress syndrome</topic><topic>Alveoli</topic><topic>Animals</topic><topic>Bronchoalveolar Lavage Fluid</topic><topic>Bronchus</topic><topic>Care and treatment</topic><topic>Chemokines</topic><topic>Chemotaxis</topic><topic>Cytokines</topic><topic>Development and progression</topic><topic>Disease Models, Animal</topic><topic>Edema</topic><topic>Gene expression</topic><topic>gene expression profiles</topic><topic>Gene Expression Regulation</topic><topic>Gene Ontology</topic><topic>Genetic aspects</topic><topic>Genomes</topic><topic>Genotype</topic><topic>Health aspects</topic><topic>Histopathology</topic><topic>Hypoxemia</topic><topic>IL-6</topic><topic>Interleukin 6</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Lungs</topic><topic>Male</topic><topic>Neutrophils</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Seawater - adverse effects</topic><topic>seawater aspiration-induced ALI</topic><topic>Sepsis</topic><topic>TNFSF10</topic><topic>Transcription</topic><topic>Transcriptome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Wei</creatorcontrib><creatorcontrib>Pan, Lei</creatorcontrib><creatorcontrib>Zhang, Minlong</creatorcontrib><creatorcontrib>Bo, Liyan</creatorcontrib><creatorcontrib>Li, Congcong</creatorcontrib><creatorcontrib>Liu, Qingqing</creatorcontrib><creatorcontrib>Wang, Li</creatorcontrib><creatorcontrib>Jin, Faguang</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</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>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</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>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Wei</au><au>Pan, Lei</au><au>Zhang, Minlong</au><au>Bo, Liyan</au><au>Li, Congcong</au><au>Liu, Qingqing</au><au>Wang, Li</au><au>Jin, Faguang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identification of distinct genes associated with seawater aspiration-induced acute lung injury by gene expression profile analysis</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2016-10-01</date><risdate>2016</risdate><volume>14</volume><issue>4</issue><spage>3168</spage><epage>3178</epage><pages>3168-3178</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Seawater aspiration-induced acute lung injury (ALI) is a syndrome associated with a high mortality rate, which is characterized by severe hypoxemia, pulmonary edema and inflammation. The present study is the first, to the best of our knowledge, to analyze gene expression profiles from a rat model of seawater aspiration-induced ALI. Adult male Sprague-Dawley rats were instilled with seawater (4 ml/kg) in the seawater aspiration-induced ALI group (S group) or with distilled water (4 ml/kg) in the distilled water negative control group (D group). In the blank control group (C group) the rats' tracheae were exposed without instillation. Subsequently, lung samples were examined by histopathology; total protein concentration was detected in bronchoalveolar lavage fluid (BALF); lung wet/dry weight ratios were determined; and transcript expression was detected by gene sequencing analysis. The results demonstrated that histopathological alterations, pulmonary edema and total protein concentrations in BALF were increased in the S group compared with in the D group. Analysis of differential gene expression identified up and downregulated genes in the S group compared with in the D and C groups. A gene ontology analysis of the differential gene expression revealed enrichment of genes in the functional pathways associated with neutrophil chemotaxis, immune and defense responses, and cytokine activity. Kyoto Encyclopedia of Genes and Genomes analysis revealed that the cytokine-cytokine receptor interaction pathway was one of the most important pathways involved in seawater aspiration-induced ALI. In conclusion, activation of the cytokine-cytokine receptor interaction pathway may have an essential role in the progression of seawater aspiration-induced ALI, and the downregulation of tumor necrosis factor superfamily member 10 may enhance inflammation. Furthermore, IL-6 may be considered a biomarker in seawater aspiration-induced ALI.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>27509884</pmid><doi>10.3892/mmr.2016.5607</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acute Lung Injury - genetics Acute Lung Injury - pathology Acute respiratory distress syndrome Alveoli Animals Bronchoalveolar Lavage Fluid Bronchus Care and treatment Chemokines Chemotaxis Cytokines Development and progression Disease Models, Animal Edema Gene expression gene expression profiles Gene Expression Regulation Gene Ontology Genetic aspects Genomes Genotype Health aspects Histopathology Hypoxemia IL-6 Interleukin 6 Kinases Laboratory animals Lung - metabolism Lung - pathology Lungs Male Neutrophils Rats, Sprague-Dawley Rodents Seawater - adverse effects seawater aspiration-induced ALI Sepsis TNFSF10 Transcription Transcriptome |
title | Identification of distinct genes associated with seawater aspiration-induced acute lung injury by gene expression profile analysis |
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