High-altitude pulmonary hypertension in cattle (brisket disease): Candidate genes and gene expression profiling of peripheral blood mononuclear cells
High-altitude pulmonary hypertension (HAPH) is a consequence of chronic alveolar hypoxia, leading to hypoxic vasoconstriction and remodeling of the pulmonary circulation. Brisket disease in cattle is a naturally occurring animal model of hypoxic pulmonary hypertension. Genetically susceptible cattle...
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| Veröffentlicht in: | Pulmonary circulation 2011-10, Vol.1 (4), p.462-469 |
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| description | High-altitude pulmonary hypertension (HAPH) is a consequence of chronic alveolar hypoxia, leading to hypoxic vasoconstriction and remodeling of the pulmonary circulation. Brisket disease in cattle is a naturally occurring animal model of hypoxic pulmonary hypertension. Genetically susceptible cattle develop severe pulmonary hypertension and right heart failure at altitudes >7,000 ft. No information currently exists regarding the identity of the pathways and gene(s) responsible for HAPH or influencing severity. We hypothesized that initial insights into the pathogenesis of the disease could be discovered by a strategy of (1) sequencing of functional candidates revealed by single nucleotide polymorphism (SNP) analysis and (2) gene expression profiling of affected cattle compared with altitude-matched normal controls, with gene set enrichment analysis (GSEA) and Ingenuity pathway analysis (IPA). We isolated blood from a single herd of Black Angus cattle of both genders, aged 12–18 months, by jugular vein puncture. Mean pulmonary arterial pressures were 85.6±13 mmHg STD in the 10 affected and 35.3±1.2 mmHg STD in the 10 resistant cattle, P |
| doi_str_mv | 10.4103/2045-8932.93545 |
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Brisket disease in cattle is a naturally occurring animal model of hypoxic pulmonary hypertension. Genetically susceptible cattle develop severe pulmonary hypertension and right heart failure at altitudes >7,000 ft. No information currently exists regarding the identity of the pathways and gene(s) responsible for HAPH or influencing severity. We hypothesized that initial insights into the pathogenesis of the disease could be discovered by a strategy of (1) sequencing of functional candidates revealed by single nucleotide polymorphism (SNP) analysis and (2) gene expression profiling of affected cattle compared with altitude-matched normal controls, with gene set enrichment analysis (GSEA) and Ingenuity pathway analysis (IPA). We isolated blood from a single herd of Black Angus cattle of both genders, aged 12–18 months, by jugular vein puncture. Mean pulmonary arterial pressures were 85.6±13 mmHg STD in the 10 affected and 35.3±1.2 mmHg STD in the 10 resistant cattle, P<0.001. From peripheral blood mononuclear cells, DNA was hybridized to an Affymetrix 10K Gene Chip SNP, and RNA was used to probe an Affymetrix Bovine genome array. SNP loci were remapped using the Btau 4.0 bovine genome assembly. mRNA data was analyzed by the Partek software package to identify sets of genes with an expression that was statistically different between the two groups. GSEA and IPA were conducted on the refined expression data to identify key cellular pathways and to generate networks and conduct functional analyses of the pathways and networks. Ten SNPs were identified by allelelic association and four candidate genes were sequenced in the cohort. Neither endothelial nitric oxide synthetase, NADH dehydrogenase, TG-interacting factor-2 nor BMPR2 were different among affected and resistant cattle. A 60-gene mRNA signature was identified that differentiated affected from unaffected cattle. Forty-six genes were overexpressed in the affected and 14 genes were downregulated in the affected cattle by at least 20%. GSEA and Ingenuity analysis identified respiratory diseases, inflammatory diseases and pathways as the top diseases and disorders (P<5.14×10–14), cell development and cell signaling as the top cellular functions (P<1.20×10–08), and IL6, TREM, PPAR, NFkB cell signaling (P<8.69×10–09) as the top canonical pathways associated with this gene signature. This study provides insights into differences in RNA expression in HAPH at a molecular level, and eliminates four functional gene candidates. Further studies are needed to validate and refine these preliminary findings and to determine the role of transcribed genes in the development of HAPH.</description><identifier>ISSN: 2045-8932</identifier><identifier>ISSN: 2045-8940</identifier><identifier>EISSN: 2045-8940</identifier><identifier>DOI: 10.4103/2045-8932.93545</identifier><identifier>PMID: 22530101</identifier><language>eng</language><publisher>London, England: University of Chicago Press</publisher><subject>Altitude ; Beef cattle ; brisket disease ; Cattle ; Disease ; Disease resistance ; Disease susceptibility ; Gene expression ; Genes ; Genetic diseases ; Genomes ; Hematologic diseases ; Hypertension ; Hypoxia ; Lung diseases ; microarray analysis ; Pulmonary hypertension ; Research Article ; Ungulates</subject><ispartof>Pulmonary circulation, 2011-10, Vol.1 (4), p.462-469</ispartof><rights>2011 by the Pulmonary Vascular Research Institute. All rights reserved.</rights><rights>2011 SAGE Publications Ltd, or Pulmonary Vascular Research Institute, unless otherwise noted. Manuscript content on this site is licensed under Creative Commons Licenses</rights><rights>The Author(s)</rights><rights>COPYRIGHT 2011 Sage Publications Ltd. (UK)</rights><rights>2011 SAGE Publications Ltd, or Pulmonary Vascular Research Institute, unless otherwise noted. Manuscript content on this site is licensed under Creative Commons Licenses. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the associated terms available at: https://uk.sagepub.com/en-gb/eur/reusing-open-access-and-sage-choice-content</rights><rights>Copyright: © Pulmonary Circulation 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6726-389113f1141efdd3a2cbda0761893b4711fbbce09cf812f08b77b385569b7b0b3</citedby><cites>FETCH-LOGICAL-c6726-389113f1141efdd3a2cbda0761893b4711fbbce09cf812f08b77b385569b7b0b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3329076/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3329076/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,11541,25332,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.4103%2F2045-8932.93545$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22530101$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Newman, John H.</creatorcontrib><creatorcontrib>Holt, Timothy N.</creatorcontrib><creatorcontrib>Hedges, Lora K.</creatorcontrib><creatorcontrib>Womack, Bethany</creatorcontrib><creatorcontrib>Memon, Shafia S.</creatorcontrib><creatorcontrib>Willers, Elisabeth D.</creatorcontrib><creatorcontrib>Wheeler, Lisa</creatorcontrib><creatorcontrib>Phillips, John A.</creatorcontrib><creatorcontrib>Hamid, Rizwan</creatorcontrib><title>High-altitude pulmonary hypertension in cattle (brisket disease): Candidate genes and gene expression profiling of peripheral blood mononuclear cells</title><title>Pulmonary circulation</title><addtitle>Pulm Circ</addtitle><description>High-altitude pulmonary hypertension (HAPH) is a consequence of chronic alveolar hypoxia, leading to hypoxic vasoconstriction and remodeling of the pulmonary circulation. Brisket disease in cattle is a naturally occurring animal model of hypoxic pulmonary hypertension. Genetically susceptible cattle develop severe pulmonary hypertension and right heart failure at altitudes >7,000 ft. No information currently exists regarding the identity of the pathways and gene(s) responsible for HAPH or influencing severity. We hypothesized that initial insights into the pathogenesis of the disease could be discovered by a strategy of (1) sequencing of functional candidates revealed by single nucleotide polymorphism (SNP) analysis and (2) gene expression profiling of affected cattle compared with altitude-matched normal controls, with gene set enrichment analysis (GSEA) and Ingenuity pathway analysis (IPA). We isolated blood from a single herd of Black Angus cattle of both genders, aged 12–18 months, by jugular vein puncture. Mean pulmonary arterial pressures were 85.6±13 mmHg STD in the 10 affected and 35.3±1.2 mmHg STD in the 10 resistant cattle, P<0.001. From peripheral blood mononuclear cells, DNA was hybridized to an Affymetrix 10K Gene Chip SNP, and RNA was used to probe an Affymetrix Bovine genome array. SNP loci were remapped using the Btau 4.0 bovine genome assembly. mRNA data was analyzed by the Partek software package to identify sets of genes with an expression that was statistically different between the two groups. GSEA and IPA were conducted on the refined expression data to identify key cellular pathways and to generate networks and conduct functional analyses of the pathways and networks. Ten SNPs were identified by allelelic association and four candidate genes were sequenced in the cohort. Neither endothelial nitric oxide synthetase, NADH dehydrogenase, TG-interacting factor-2 nor BMPR2 were different among affected and resistant cattle. A 60-gene mRNA signature was identified that differentiated affected from unaffected cattle. Forty-six genes were overexpressed in the affected and 14 genes were downregulated in the affected cattle by at least 20%. GSEA and Ingenuity analysis identified respiratory diseases, inflammatory diseases and pathways as the top diseases and disorders (P<5.14×10–14), cell development and cell signaling as the top cellular functions (P<1.20×10–08), and IL6, TREM, PPAR, NFkB cell signaling (P<8.69×10–09) as the top canonical pathways associated with this gene signature. This study provides insights into differences in RNA expression in HAPH at a molecular level, and eliminates four functional gene candidates. Further studies are needed to validate and refine these preliminary findings and to determine the role of transcribed genes in the development of HAPH.</description><subject>Altitude</subject><subject>Beef cattle</subject><subject>brisket disease</subject><subject>Cattle</subject><subject>Disease</subject><subject>Disease resistance</subject><subject>Disease susceptibility</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic diseases</subject><subject>Genomes</subject><subject>Hematologic diseases</subject><subject>Hypertension</subject><subject>Hypoxia</subject><subject>Lung diseases</subject><subject>microarray analysis</subject><subject>Pulmonary hypertension</subject><subject>Research Article</subject><subject>Ungulates</subject><issn>2045-8932</issn><issn>2045-8940</issn><issn>2045-8940</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>JFNAL</sourceid><sourceid>BENPR</sourceid><recordid>eNqVkl9v0zAUxSMEYtPYM2_IEi9DIp3_JE3CA9KoGEOqBA_s2bKd69QltYOdAP0gfF-cpus2BJqIpcRJfudc36uTJM8JnmUEs3OKszwtK0ZnFcuz_FFyvP-S4ceHPaNHyWkIaxyvrCIUl0-TI0pzhgkmx8mvK9OsUtH2ph9qQN3QbpwVfotW2w58DzYYZ5GxSIm-bwGdSW_CV-hRbQKIAK_eoIWwtalFD6gBCwHF190Owc_OQ9gZdN5p0xrbIKdRNDbdCrxokWydq1Es6eygWhAeKWjb8Cx5okUb4HT_PEmuL99_WVyly08fPi4ulqmaF3SesrIihGlCMgK6rpmgStYCF3MS-5ZZQYiWUgGulC4J1biURSFZmefzShYSS3aSvJ18u0FuoFZg-3gq3nmziTPgThh-_481K96475wxWsU60eBsb-DdtwFCzzcmjC0IC24InGBc5Szes4i-_ANdu8Hb2B6nLGOYRj96SzWiBW6sdrGuGk35BS0zUhWkLCM1-wsVVw0bo5yFOGy4LzifBMq7EDzoQ48E8zFMfIwLH-PCd2GKihd3R3Pgb6ITgXICfsRa24f8-OfrJX13OaZwnBqZpINaGSUat8vJnXncRHev7WodNen_aCL_euKDaOAW-3e7e3wdeucfnM5v0owPqg</recordid><startdate>201110</startdate><enddate>201110</enddate><creator>Newman, John H.</creator><creator>Holt, Timothy N.</creator><creator>Hedges, Lora K.</creator><creator>Womack, Bethany</creator><creator>Memon, Shafia S.</creator><creator>Willers, Elisabeth D.</creator><creator>Wheeler, Lisa</creator><creator>Phillips, John A.</creator><creator>Hamid, Rizwan</creator><general>University of Chicago Press</general><general>SAGE Publications</general><general>Sage Publications Ltd. (UK)</general><general>John Wiley & Sons, Inc</general><general>Medknow Publications & Media Pvt Ltd</general><scope>JFNAL</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201110</creationdate><title>High-altitude pulmonary hypertension in cattle (brisket disease): Candidate genes and gene expression profiling of peripheral blood mononuclear cells</title><author>Newman, John H. ; Holt, Timothy N. ; Hedges, Lora K. ; Womack, Bethany ; Memon, Shafia S. ; Willers, Elisabeth D. ; Wheeler, Lisa ; Phillips, John A. ; Hamid, Rizwan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6726-389113f1141efdd3a2cbda0761893b4711fbbce09cf812f08b77b385569b7b0b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Altitude</topic><topic>Beef cattle</topic><topic>brisket disease</topic><topic>Cattle</topic><topic>Disease</topic><topic>Disease resistance</topic><topic>Disease susceptibility</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Genetic diseases</topic><topic>Genomes</topic><topic>Hematologic diseases</topic><topic>Hypertension</topic><topic>Hypoxia</topic><topic>Lung diseases</topic><topic>microarray analysis</topic><topic>Pulmonary hypertension</topic><topic>Research Article</topic><topic>Ungulates</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Newman, John H.</creatorcontrib><creatorcontrib>Holt, Timothy N.</creatorcontrib><creatorcontrib>Hedges, Lora K.</creatorcontrib><creatorcontrib>Womack, Bethany</creatorcontrib><creatorcontrib>Memon, Shafia S.</creatorcontrib><creatorcontrib>Willers, Elisabeth D.</creatorcontrib><creatorcontrib>Wheeler, Lisa</creatorcontrib><creatorcontrib>Phillips, John A.</creatorcontrib><creatorcontrib>Hamid, Rizwan</creatorcontrib><collection>Jstor Journals Open Access</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>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>ProQuest Central Essentials</collection><collection>ProQuest Central</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 Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Publicly Available Content 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>Pulmonary circulation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Newman, John H.</au><au>Holt, Timothy N.</au><au>Hedges, Lora K.</au><au>Womack, Bethany</au><au>Memon, Shafia S.</au><au>Willers, Elisabeth D.</au><au>Wheeler, Lisa</au><au>Phillips, John A.</au><au>Hamid, Rizwan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High-altitude pulmonary hypertension in cattle (brisket disease): Candidate genes and gene expression profiling of peripheral blood mononuclear cells</atitle><jtitle>Pulmonary circulation</jtitle><addtitle>Pulm Circ</addtitle><date>2011-10</date><risdate>2011</risdate><volume>1</volume><issue>4</issue><spage>462</spage><epage>469</epage><pages>462-469</pages><issn>2045-8932</issn><issn>2045-8940</issn><eissn>2045-8940</eissn><abstract>High-altitude pulmonary hypertension (HAPH) is a consequence of chronic alveolar hypoxia, leading to hypoxic vasoconstriction and remodeling of the pulmonary circulation. Brisket disease in cattle is a naturally occurring animal model of hypoxic pulmonary hypertension. Genetically susceptible cattle develop severe pulmonary hypertension and right heart failure at altitudes >7,000 ft. No information currently exists regarding the identity of the pathways and gene(s) responsible for HAPH or influencing severity. We hypothesized that initial insights into the pathogenesis of the disease could be discovered by a strategy of (1) sequencing of functional candidates revealed by single nucleotide polymorphism (SNP) analysis and (2) gene expression profiling of affected cattle compared with altitude-matched normal controls, with gene set enrichment analysis (GSEA) and Ingenuity pathway analysis (IPA). We isolated blood from a single herd of Black Angus cattle of both genders, aged 12–18 months, by jugular vein puncture. Mean pulmonary arterial pressures were 85.6±13 mmHg STD in the 10 affected and 35.3±1.2 mmHg STD in the 10 resistant cattle, P<0.001. From peripheral blood mononuclear cells, DNA was hybridized to an Affymetrix 10K Gene Chip SNP, and RNA was used to probe an Affymetrix Bovine genome array. SNP loci were remapped using the Btau 4.0 bovine genome assembly. mRNA data was analyzed by the Partek software package to identify sets of genes with an expression that was statistically different between the two groups. GSEA and IPA were conducted on the refined expression data to identify key cellular pathways and to generate networks and conduct functional analyses of the pathways and networks. Ten SNPs were identified by allelelic association and four candidate genes were sequenced in the cohort. Neither endothelial nitric oxide synthetase, NADH dehydrogenase, TG-interacting factor-2 nor BMPR2 were different among affected and resistant cattle. A 60-gene mRNA signature was identified that differentiated affected from unaffected cattle. Forty-six genes were overexpressed in the affected and 14 genes were downregulated in the affected cattle by at least 20%. GSEA and Ingenuity analysis identified respiratory diseases, inflammatory diseases and pathways as the top diseases and disorders (P<5.14×10–14), cell development and cell signaling as the top cellular functions (P<1.20×10–08), and IL6, TREM, PPAR, NFkB cell signaling (P<8.69×10–09) as the top canonical pathways associated with this gene signature. This study provides insights into differences in RNA expression in HAPH at a molecular level, and eliminates four functional gene candidates. Further studies are needed to validate and refine these preliminary findings and to determine the role of transcribed genes in the development of HAPH.</abstract><cop>London, England</cop><pub>University of Chicago Press</pub><pmid>22530101</pmid><doi>10.4103/2045-8932.93545</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Altitude Beef cattle brisket disease Cattle Disease Disease resistance Disease susceptibility Gene expression Genes Genetic diseases Genomes Hematologic diseases Hypertension Hypoxia Lung diseases microarray analysis Pulmonary hypertension Research Article Ungulates |
| title | High-altitude pulmonary hypertension in cattle (brisket disease): Candidate genes and gene expression profiling of peripheral blood mononuclear cells |
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