A temporal study of gene expression in rat lung following fixed-volume hemorrhage
United States Army Institute of Surgical Research, Fort Sam Houston, Texas Previous studies have indicated that hemorrhage may predispose the lung to respiratory distress syndrome. Gene expression profiling with oligonucleotide microarrays was used to evaluate the genetic responses of the lung to he...
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Veröffentlicht in: | Physiological genomics 2005-11, Vol.23 (3), p.275-286 |
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creator | Bowman, P. D Sondeen, J. L Zhao, B Coppes, V. G Nelson, J. J Dubick, M. A Vaughan, G. M |
description | United States Army Institute of Surgical Research, Fort Sam Houston, Texas
Previous studies have indicated that hemorrhage may predispose the lung to respiratory distress syndrome. Gene expression profiling with oligonucleotide microarrays was used to evaluate the genetic responses of the lung to hemorrhage. Conscious rats, chronically instrumented with a catheter and telemetry device to record blood pressure, heart rate, and temperature, had 40% of their estimated blood volume removed at a rate of 1 ml/min over 710 min. Groups of three or more rats were euthanized at 1, 3, 6, 16, 24, 48, or 72 h following hemorrhage. Two additional groups were unmanipulated controls and instrumented animals with sham hemorrhage. Total RNA was isolated from lung, reverse-transcribed to cDNA, fluorescently labeled, and hybridized to oligonucleotide microarrays probing 5,671 rat genes. After hemorrhage, statistically detectable alteration of expression was seen in 0.8% of the genes at some time during the 72-h test period (vs. sham hemorrhage) as determined by false discovery rate statistics in the statistical analysis of microarrays program. A subset was confirmed by RT-PCR analysis. Hemorrhage influenced genes that regulate intracellular signaling and structure, growth factors, and hormonal receptors. There also appeared to be increased expression of genes that may mediate sequestration of neutrophils and mononuclear cells from the circulation. This hemorrhage model, although producing severe hemodynamic alterations, avoided mortality and histological evidence of lung damage, a feature intended to help ensure reliable evaluation of gene expression. These results indicate that gene expression profiling with microarrays provides a new tool for exploring the response of a tissue to systemic blood loss.
gene expression profiling; ischemic lung injury |
doi_str_mv | 10.1152/physiolgenomics.00075.2005 |
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Previous studies have indicated that hemorrhage may predispose the lung to respiratory distress syndrome. Gene expression profiling with oligonucleotide microarrays was used to evaluate the genetic responses of the lung to hemorrhage. Conscious rats, chronically instrumented with a catheter and telemetry device to record blood pressure, heart rate, and temperature, had 40% of their estimated blood volume removed at a rate of 1 ml/min over 710 min. Groups of three or more rats were euthanized at 1, 3, 6, 16, 24, 48, or 72 h following hemorrhage. Two additional groups were unmanipulated controls and instrumented animals with sham hemorrhage. Total RNA was isolated from lung, reverse-transcribed to cDNA, fluorescently labeled, and hybridized to oligonucleotide microarrays probing 5,671 rat genes. After hemorrhage, statistically detectable alteration of expression was seen in 0.8% of the genes at some time during the 72-h test period (vs. sham hemorrhage) as determined by false discovery rate statistics in the statistical analysis of microarrays program. A subset was confirmed by RT-PCR analysis. Hemorrhage influenced genes that regulate intracellular signaling and structure, growth factors, and hormonal receptors. There also appeared to be increased expression of genes that may mediate sequestration of neutrophils and mononuclear cells from the circulation. This hemorrhage model, although producing severe hemodynamic alterations, avoided mortality and histological evidence of lung damage, a feature intended to help ensure reliable evaluation of gene expression. These results indicate that gene expression profiling with microarrays provides a new tool for exploring the response of a tissue to systemic blood loss.
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Previous studies have indicated that hemorrhage may predispose the lung to respiratory distress syndrome. Gene expression profiling with oligonucleotide microarrays was used to evaluate the genetic responses of the lung to hemorrhage. Conscious rats, chronically instrumented with a catheter and telemetry device to record blood pressure, heart rate, and temperature, had 40% of their estimated blood volume removed at a rate of 1 ml/min over 710 min. Groups of three or more rats were euthanized at 1, 3, 6, 16, 24, 48, or 72 h following hemorrhage. Two additional groups were unmanipulated controls and instrumented animals with sham hemorrhage. Total RNA was isolated from lung, reverse-transcribed to cDNA, fluorescently labeled, and hybridized to oligonucleotide microarrays probing 5,671 rat genes. After hemorrhage, statistically detectable alteration of expression was seen in 0.8% of the genes at some time during the 72-h test period (vs. sham hemorrhage) as determined by false discovery rate statistics in the statistical analysis of microarrays program. A subset was confirmed by RT-PCR analysis. Hemorrhage influenced genes that regulate intracellular signaling and structure, growth factors, and hormonal receptors. There also appeared to be increased expression of genes that may mediate sequestration of neutrophils and mononuclear cells from the circulation. This hemorrhage model, although producing severe hemodynamic alterations, avoided mortality and histological evidence of lung damage, a feature intended to help ensure reliable evaluation of gene expression. These results indicate that gene expression profiling with microarrays provides a new tool for exploring the response of a tissue to systemic blood loss.
gene expression profiling; ischemic lung injury</description><subject>Animals</subject><subject>Blood Proteins - metabolism</subject><subject>DNA Primers</subject><subject>Gene Expression Regulation</subject><subject>Hemodynamics</subject><subject>Hemorrhage - blood</subject><subject>Hemorrhage - genetics</subject><subject>Lung - physiopathology</subject><subject>Male</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA - genetics</subject><subject>RNA - isolation & purification</subject><subject>Shock - epidemiology</subject><subject>Transcription, Genetic</subject><issn>1094-8341</issn><issn>1531-2267</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1r1UAUhgex2Nr6F2Rw4S7X-U7GjZRiVShIoV0PczMnycgkE2eS9t5_b-K9RaiIq_Mu3uc98CD0jpINpZJ9GLt99jG0MMTe13lDCCnlhhEiX6AzKjktGFPlyyUTLYqKC3qKXuf8gxAqykq-QqdUUak1JWfo9hJP0I8x2YDzNLs9jg1elgHDbkyQl0cD9gNOdsJhHlrcxBDio1-T34ErHmKYe8Ad9DGlzrZwgU4aGzK8Od5zdH_9-e7qa3Hz_cu3q8ubohaimopaCea2NWuU04pSJmpeAwG31YLVxEoprRKacd7QkmjrKqqcYFxLDSA5c_wcvT_sjin-nCFPpve5hhDsAHHORlUVLbki_y1Svapgeil-PBTrFHNO0Jgx-d6mvaHErObNM_Pmt3mzml_gt8cv87YH9wc9ql4K_FDofNs9-gRPa7Hd_zXMuOGGlevsp39T13MId7CbnuNPtBldw38Bw1ewNQ</recordid><startdate>20051117</startdate><enddate>20051117</enddate><creator>Bowman, P. D</creator><creator>Sondeen, J. L</creator><creator>Zhao, B</creator><creator>Coppes, V. G</creator><creator>Nelson, J. J</creator><creator>Dubick, M. A</creator><creator>Vaughan, G. M</creator><general>Am Physiological Soc</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20051117</creationdate><title>A temporal study of gene expression in rat lung following fixed-volume hemorrhage</title><author>Bowman, P. D ; Sondeen, J. L ; Zhao, B ; Coppes, V. G ; Nelson, J. J ; Dubick, M. A ; Vaughan, G. M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-c642dbc2f6d961124c3ce0edb942c0a555a649233f1709ad816d423959ee532d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Blood Proteins - metabolism</topic><topic>DNA Primers</topic><topic>Gene Expression Regulation</topic><topic>Hemodynamics</topic><topic>Hemorrhage - blood</topic><topic>Hemorrhage - genetics</topic><topic>Lung - physiopathology</topic><topic>Male</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA - genetics</topic><topic>RNA - isolation & purification</topic><topic>Shock - epidemiology</topic><topic>Transcription, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bowman, P. D</creatorcontrib><creatorcontrib>Sondeen, J. L</creatorcontrib><creatorcontrib>Zhao, B</creatorcontrib><creatorcontrib>Coppes, V. G</creatorcontrib><creatorcontrib>Nelson, J. J</creatorcontrib><creatorcontrib>Dubick, M. A</creatorcontrib><creatorcontrib>Vaughan, G. M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Physiological genomics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bowman, P. D</au><au>Sondeen, J. L</au><au>Zhao, B</au><au>Coppes, V. G</au><au>Nelson, J. J</au><au>Dubick, M. A</au><au>Vaughan, G. M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A temporal study of gene expression in rat lung following fixed-volume hemorrhage</atitle><jtitle>Physiological genomics</jtitle><addtitle>Physiol Genomics</addtitle><date>2005-11-17</date><risdate>2005</risdate><volume>23</volume><issue>3</issue><spage>275</spage><epage>286</epage><pages>275-286</pages><issn>1094-8341</issn><eissn>1531-2267</eissn><abstract>United States Army Institute of Surgical Research, Fort Sam Houston, Texas
Previous studies have indicated that hemorrhage may predispose the lung to respiratory distress syndrome. Gene expression profiling with oligonucleotide microarrays was used to evaluate the genetic responses of the lung to hemorrhage. Conscious rats, chronically instrumented with a catheter and telemetry device to record blood pressure, heart rate, and temperature, had 40% of their estimated blood volume removed at a rate of 1 ml/min over 710 min. Groups of three or more rats were euthanized at 1, 3, 6, 16, 24, 48, or 72 h following hemorrhage. Two additional groups were unmanipulated controls and instrumented animals with sham hemorrhage. Total RNA was isolated from lung, reverse-transcribed to cDNA, fluorescently labeled, and hybridized to oligonucleotide microarrays probing 5,671 rat genes. After hemorrhage, statistically detectable alteration of expression was seen in 0.8% of the genes at some time during the 72-h test period (vs. sham hemorrhage) as determined by false discovery rate statistics in the statistical analysis of microarrays program. A subset was confirmed by RT-PCR analysis. Hemorrhage influenced genes that regulate intracellular signaling and structure, growth factors, and hormonal receptors. There also appeared to be increased expression of genes that may mediate sequestration of neutrophils and mononuclear cells from the circulation. This hemorrhage model, although producing severe hemodynamic alterations, avoided mortality and histological evidence of lung damage, a feature intended to help ensure reliable evaluation of gene expression. These results indicate that gene expression profiling with microarrays provides a new tool for exploring the response of a tissue to systemic blood loss.
gene expression profiling; ischemic lung injury</abstract><cop>United States</cop><pub>Am Physiological Soc</pub><pmid>16159910</pmid><doi>10.1152/physiolgenomics.00075.2005</doi><tpages>12</tpages></addata></record> |
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subjects | Animals Blood Proteins - metabolism DNA Primers Gene Expression Regulation Hemodynamics Hemorrhage - blood Hemorrhage - genetics Lung - physiopathology Male Oligonucleotide Array Sequence Analysis Rats Rats, Sprague-Dawley Reverse Transcriptase Polymerase Chain Reaction RNA - genetics RNA - isolation & purification Shock - epidemiology Transcription, Genetic |
title | A temporal study of gene expression in rat lung following fixed-volume hemorrhage |
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