Proteomic analysis of pulmonary arteries and lung tissues from dogs affected with pulmonary hypertension secondary to degenerative mitral valve disease
In dogs with degenerative mitral valve disease (DMVD), pulmonary hypertension (PH) is a common complication characterized by abnormally elevated pulmonary arterial pressure (PAP). Pulmonary arterial remodeling is the histopathological changes of pulmonary artery that has been recognized in PH. The u...
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| creator | Sakarin, Siriwan Rungsipipat, Anudep Roytrakul, Sittiruk Jaresitthikunchai, Janthima Phaonakrop, Narumon Charoenlappanit, Sawanya Thaisakun, Siriwan Surachetpong, Sirilak Disatian |
| description | In dogs with degenerative mitral valve disease (DMVD), pulmonary hypertension (PH) is a common complication characterized by abnormally elevated pulmonary arterial pressure (PAP). Pulmonary arterial remodeling is the histopathological changes of pulmonary artery that has been recognized in PH. The underlying mechanisms that cause this arterial remodeling are poorly understood. This study aimed to perform shotgun proteomics to investigate changes in protein expression in pulmonary arteries and lung tissues of DMVD dogs with PH compared to normal control dogs and DMVD dogs without PH. Tissue samples were collected from the carcasses of 22 small-sized breed dogs and divided into three groups: control (n = 7), DMVD (n = 7) and DMVD+PH groups (n = 8). Differentially expressed proteins were identified, and top three upregulated and downregulated proteins in the pulmonary arteries of DMVD dogs with PH including SIK family kinase 3 (SIK3), Collagen type I alpha 1 chain (COL1A1), Transforming growth factor alpha (TGF-α), Apoptosis associated tyrosine kinase (AATYK), Hepatocyte growth factor activator (HGFA) and Tyrosine-protein phosphatase non-receptor type 13 (PTPN13) were chosen. Results showed that some of the identified proteins may play a role in the pathogenesis of pulmonary arterial remodeling. This study concluded shotgun proteomics has potential as a tool for exploring candidate proteins associated with the pathogenesis of PH secondary to DMVD in dogs. |
| doi_str_mv | 10.1371/journal.pone.0296068 |
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Pulmonary arterial remodeling is the histopathological changes of pulmonary artery that has been recognized in PH. The underlying mechanisms that cause this arterial remodeling are poorly understood. This study aimed to perform shotgun proteomics to investigate changes in protein expression in pulmonary arteries and lung tissues of DMVD dogs with PH compared to normal control dogs and DMVD dogs without PH. Tissue samples were collected from the carcasses of 22 small-sized breed dogs and divided into three groups: control (n = 7), DMVD (n = 7) and DMVD+PH groups (n = 8). Differentially expressed proteins were identified, and top three upregulated and downregulated proteins in the pulmonary arteries of DMVD dogs with PH including SIK family kinase 3 (SIK3), Collagen type I alpha 1 chain (COL1A1), Transforming growth factor alpha (TGF-α), Apoptosis associated tyrosine kinase (AATYK), Hepatocyte growth factor activator (HGFA) and Tyrosine-protein phosphatase non-receptor type 13 (PTPN13) were chosen. Results showed that some of the identified proteins may play a role in the pathogenesis of pulmonary arterial remodeling. This study concluded shotgun proteomics has potential as a tool for exploring candidate proteins associated with the pathogenesis of PH secondary to DMVD in dogs.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0296068</identifier><identifier>PMID: 38181036</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animals ; Apoptosis ; Arteries ; Blood pressure ; Chromatography ; Collagen (type I) ; Comparative analysis ; Complications and side effects ; Development and progression ; Diagnosis ; Disease ; Dogs ; Down-regulation ; Growth factors ; Health aspects ; Heart failure ; Heart valve diseases ; Hepatocyte growth factor ; Hypertension ; Hypertension, Pulmonary - veterinary ; Kinases ; Lung ; Lung diseases ; Lungs ; Mass spectrometry ; Medical records ; Mitral Valve ; Pathogenesis ; Phosphatases ; Protein phosphatase ; Protein-tyrosine-phosphatase ; Proteins ; Proteomics ; Pulmonary arteries ; Pulmonary Artery ; Pulmonary hypertension ; Rheumatic heart disease ; Scientific imaging ; Shotguns ; Transforming growth factor-a ; Transforming growth factors ; Tyrosine ; Variance analysis ; Vascular Remodeling ; Veins & arteries</subject><ispartof>PloS one, 2024-01, Vol.19 (1), p.e0296068-e0296068</ispartof><rights>Copyright: © 2024 Sakarin et al. 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This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c637t-f3c2a207e5e6b1b3753931e462096dd11118386f17558302c07a62d6c1f369e3</citedby><cites>FETCH-LOGICAL-c637t-f3c2a207e5e6b1b3753931e462096dd11118386f17558302c07a62d6c1f369e3</cites><orcidid>0000-0001-5041-7849</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0296068&type=printable$$EPDF$$P50$$Gplos$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0296068$$EHTML$$P50$$Gplos$$Hfree_for_read</linktohtml><link.rule.ids>314,777,781,861,2096,2915,23847,27905,27906,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38181036$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Maloney, James P.</contributor><creatorcontrib>Sakarin, Siriwan</creatorcontrib><creatorcontrib>Rungsipipat, Anudep</creatorcontrib><creatorcontrib>Roytrakul, Sittiruk</creatorcontrib><creatorcontrib>Jaresitthikunchai, Janthima</creatorcontrib><creatorcontrib>Phaonakrop, Narumon</creatorcontrib><creatorcontrib>Charoenlappanit, Sawanya</creatorcontrib><creatorcontrib>Thaisakun, Siriwan</creatorcontrib><creatorcontrib>Surachetpong, Sirilak Disatian</creatorcontrib><title>Proteomic analysis of pulmonary arteries and lung tissues from dogs affected with pulmonary hypertension secondary to degenerative mitral valve disease</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>In dogs with degenerative mitral valve disease (DMVD), pulmonary hypertension (PH) is a common complication characterized by abnormally elevated pulmonary arterial pressure (PAP). 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one</jtitle><addtitle>PLoS One</addtitle><date>2024-01-05</date><risdate>2024</risdate><volume>19</volume><issue>1</issue><spage>e0296068</spage><epage>e0296068</epage><pages>e0296068-e0296068</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>In dogs with degenerative mitral valve disease (DMVD), pulmonary hypertension (PH) is a common complication characterized by abnormally elevated pulmonary arterial pressure (PAP). Pulmonary arterial remodeling is the histopathological changes of pulmonary artery that has been recognized in PH. The underlying mechanisms that cause this arterial remodeling are poorly understood. This study aimed to perform shotgun proteomics to investigate changes in protein expression in pulmonary arteries and lung tissues of DMVD dogs with PH compared to normal control dogs and DMVD dogs without PH. Tissue samples were collected from the carcasses of 22 small-sized breed dogs and divided into three groups: control (n = 7), DMVD (n = 7) and DMVD+PH groups (n = 8). Differentially expressed proteins were identified, and top three upregulated and downregulated proteins in the pulmonary arteries of DMVD dogs with PH including SIK family kinase 3 (SIK3), Collagen type I alpha 1 chain (COL1A1), Transforming growth factor alpha (TGF-α), Apoptosis associated tyrosine kinase (AATYK), Hepatocyte growth factor activator (HGFA) and Tyrosine-protein phosphatase non-receptor type 13 (PTPN13) were chosen. Results showed that some of the identified proteins may play a role in the pathogenesis of pulmonary arterial remodeling. This study concluded shotgun proteomics has potential as a tool for exploring candidate proteins associated with the pathogenesis of PH secondary to DMVD in dogs.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>38181036</pmid><doi>10.1371/journal.pone.0296068</doi><tpages>e0296068</tpages><orcidid>https://orcid.org/0000-0001-5041-7849</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | PloS one, 2024-01, Vol.19 (1), p.e0296068-e0296068 |
| issn | 1932-6203 1932-6203 |
| language | eng |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Analysis Animals Apoptosis Arteries Blood pressure Chromatography Collagen (type I) Comparative analysis Complications and side effects Development and progression Diagnosis Disease Dogs Down-regulation Growth factors Health aspects Heart failure Heart valve diseases Hepatocyte growth factor Hypertension Hypertension, Pulmonary - veterinary Kinases Lung Lung diseases Lungs Mass spectrometry Medical records Mitral Valve Pathogenesis Phosphatases Protein phosphatase Protein-tyrosine-phosphatase Proteins Proteomics Pulmonary arteries Pulmonary Artery Pulmonary hypertension Rheumatic heart disease Scientific imaging Shotguns Transforming growth factor-a Transforming growth factors Tyrosine Variance analysis Vascular Remodeling Veins & arteries |
| title | Proteomic analysis of pulmonary arteries and lung tissues from dogs affected with pulmonary hypertension secondary to degenerative mitral valve disease |
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