Stability and Species Specificity of Renal VEGF-A Splicing Patterns in Kidney Disease
Vascular endothelial growth factor A (VEGF-A) is essential for maintaining the glomerular filtration barrier. Absolute renal levels of VEGF-A change in patients with diabetic nephropathy and inflammatory kidney diseases, but whether changes in the renal splicing patterns of VEGF-A play a role remain...
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| description | Vascular endothelial growth factor A (VEGF-A) is essential for maintaining the glomerular filtration barrier. Absolute renal levels of VEGF-A change in patients with diabetic nephropathy and inflammatory kidney diseases, but whether changes in the renal splicing patterns of VEGF-A play a role remains unclear. In this study, we investigated mRNA splicing patterns of pro-angiogenic isoforms of VEGF-A in glomeruli and whole kidney samples from human patients with kidney disease and from mouse models of kidney disease. Kidney biopsies were obtained from patients with acute rejection following kidney transplantation, patients with diabetic nephropathy, and control subjects. In addition, kidney samples were obtained from mice with lupus nephritis, mice with diabetes mellitus, and control mice. The relative expression of each VEGF-A splice variant was measured using RT-PCR followed by quantitative fragment analysis. The pattern of renal VEGF-A splice variants was unchanged in diabetic nephropathy and lupus nephritis and was stable throughout disease progression in acute transplant rejection and diabetic nephropathy; these results suggest renal VEGF-A splicing stability during kidney disease. The splicing patterns were species-specific; in the control human kidney samples, VEGF-A 121 was the dominant isoform, whereas VEGF-A 164 was the dominant isoform measured in the mouse kidney samples. |
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Absolute renal levels of VEGF-A change in patients with diabetic nephropathy and inflammatory kidney diseases, but whether changes in the renal splicing patterns of VEGF-A play a role remains unclear. In this study, we investigated mRNA splicing patterns of pro-angiogenic isoforms of VEGF-A in glomeruli and whole kidney samples from human patients with kidney disease and from mouse models of kidney disease. Kidney biopsies were obtained from patients with acute rejection following kidney transplantation, patients with diabetic nephropathy, and control subjects. In addition, kidney samples were obtained from mice with lupus nephritis, mice with diabetes mellitus, and control mice. The relative expression of each VEGF-A splice variant was measured using RT-PCR followed by quantitative fragment analysis. The pattern of renal VEGF-A splice variants was unchanged in diabetic nephropathy and lupus nephritis and was stable throughout disease progression in acute transplant rejection and diabetic nephropathy; these results suggest renal VEGF-A splicing stability during kidney disease. The splicing patterns were species-specific; in the control human kidney samples, VEGF-A 121 was the dominant isoform, whereas VEGF-A 164 was the dominant isoform measured in the mouse kidney samples.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0162166</identifier><identifier>PMID: 27598902</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alternative Splicing ; Analysis ; Angiogenesis ; Animal models ; Animals ; Autoimmune diseases ; Binding sites ; Biological activity ; Biology and Life Sciences ; Biopsy ; Case-Control Studies ; Control stability ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - metabolism ; Diabetes Mellitus, Type 2 - pathology ; Diabetes Mellitus, Type 2 - surgery ; Diabetic Nephropathies - genetics ; Diabetic Nephropathies - metabolism ; Diabetic Nephropathies - pathology ; Diabetic Nephropathies - surgery ; Diabetic nephropathy ; Disease control ; Disease Models, Animal ; Disease Progression ; Gene Expression ; Genetic aspects ; Graft rejection ; Graft Rejection - genetics ; Graft Rejection - immunology ; Graft Rejection - pathology ; Health aspects ; Humans ; Identification and classification ; Isoforms ; Kidney diseases ; Kidney Glomerulus - metabolism ; Kidney Glomerulus - pathology ; Kidney Transplantation ; Lupus ; Lupus nephritis ; Lupus Nephritis - genetics ; Lupus Nephritis - metabolism ; Lupus Nephritis - pathology ; Medicine and Health Sciences ; Mice ; mRNA ; Nephritis ; Nephropathy ; Pathology ; Patients ; Polymerase chain reaction ; Rejection ; Research and Analysis Methods ; Rodents ; Species Specificity ; Studies ; Transplantation ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - genetics ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>PloS one, 2016-09, Vol.11 (9), p.e0162166-e0162166</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Turner et al. 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><rights>2016 Turner et al 2016 Turner et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c725t-44ec091c3cf1a214ec60441aa23226b62fe2f1ce0d17b23ea196d0f89aebd45c3</citedby><cites>FETCH-LOGICAL-c725t-44ec091c3cf1a214ec60441aa23226b62fe2f1ce0d17b23ea196d0f89aebd45c3</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/PMC5012578/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5012578/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27598902$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Turner, R J</creatorcontrib><creatorcontrib>Eikmans, M</creatorcontrib><creatorcontrib>Bajema, I M</creatorcontrib><creatorcontrib>Bruijn, J A</creatorcontrib><creatorcontrib>Baelde, H J</creatorcontrib><title>Stability and Species Specificity of Renal VEGF-A Splicing Patterns in Kidney Disease</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Vascular endothelial growth factor A (VEGF-A) is essential for maintaining the glomerular filtration barrier. Absolute renal levels of VEGF-A change in patients with diabetic nephropathy and inflammatory kidney diseases, but whether changes in the renal splicing patterns of VEGF-A play a role remains unclear. In this study, we investigated mRNA splicing patterns of pro-angiogenic isoforms of VEGF-A in glomeruli and whole kidney samples from human patients with kidney disease and from mouse models of kidney disease. Kidney biopsies were obtained from patients with acute rejection following kidney transplantation, patients with diabetic nephropathy, and control subjects. In addition, kidney samples were obtained from mice with lupus nephritis, mice with diabetes mellitus, and control mice. The relative expression of each VEGF-A splice variant was measured using RT-PCR followed by quantitative fragment analysis. The pattern of renal VEGF-A splice variants was unchanged in diabetic nephropathy and lupus nephritis and was stable throughout disease progression in acute transplant rejection and diabetic nephropathy; these results suggest renal VEGF-A splicing stability during kidney disease. The splicing patterns were species-specific; in the control human kidney samples, VEGF-A 121 was the dominant isoform, whereas VEGF-A 164 was the dominant isoform measured in the mouse kidney samples.</description><subject>Alternative Splicing</subject><subject>Analysis</subject><subject>Angiogenesis</subject><subject>Animal models</subject><subject>Animals</subject><subject>Autoimmune diseases</subject><subject>Binding sites</subject><subject>Biological activity</subject><subject>Biology and Life Sciences</subject><subject>Biopsy</subject><subject>Case-Control Studies</subject><subject>Control stability</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - pathology</subject><subject>Diabetes Mellitus, Type 2 - surgery</subject><subject>Diabetic Nephropathies - genetics</subject><subject>Diabetic Nephropathies - metabolism</subject><subject>Diabetic Nephropathies - pathology</subject><subject>Diabetic Nephropathies - surgery</subject><subject>Diabetic nephropathy</subject><subject>Disease control</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Gene Expression</subject><subject>Genetic aspects</subject><subject>Graft rejection</subject><subject>Graft Rejection - genetics</subject><subject>Graft Rejection - immunology</subject><subject>Graft Rejection - pathology</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Identification and classification</subject><subject>Isoforms</subject><subject>Kidney diseases</subject><subject>Kidney Glomerulus - metabolism</subject><subject>Kidney Glomerulus - pathology</subject><subject>Kidney Transplantation</subject><subject>Lupus</subject><subject>Lupus nephritis</subject><subject>Lupus Nephritis - genetics</subject><subject>Lupus Nephritis - metabolism</subject><subject>Lupus Nephritis - pathology</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>mRNA</subject><subject>Nephritis</subject><subject>Nephropathy</subject><subject>Pathology</subject><subject>Patients</subject><subject>Polymerase chain reaction</subject><subject>Rejection</subject><subject>Research and Analysis Methods</subject><subject>Rodents</subject><subject>Species Specificity</subject><subject>Studies</subject><subject>Transplantation</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Turner, R J</au><au>Eikmans, M</au><au>Bajema, I M</au><au>Bruijn, J A</au><au>Baelde, H J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Stability and Species Specificity of Renal VEGF-A Splicing Patterns in Kidney Disease</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-09-06</date><risdate>2016</risdate><volume>11</volume><issue>9</issue><spage>e0162166</spage><epage>e0162166</epage><pages>e0162166-e0162166</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Vascular endothelial growth factor A (VEGF-A) is essential for maintaining the glomerular filtration barrier. Absolute renal levels of VEGF-A change in patients with diabetic nephropathy and inflammatory kidney diseases, but whether changes in the renal splicing patterns of VEGF-A play a role remains unclear. In this study, we investigated mRNA splicing patterns of pro-angiogenic isoforms of VEGF-A in glomeruli and whole kidney samples from human patients with kidney disease and from mouse models of kidney disease. Kidney biopsies were obtained from patients with acute rejection following kidney transplantation, patients with diabetic nephropathy, and control subjects. In addition, kidney samples were obtained from mice with lupus nephritis, mice with diabetes mellitus, and control mice. The relative expression of each VEGF-A splice variant was measured using RT-PCR followed by quantitative fragment analysis. The pattern of renal VEGF-A splice variants was unchanged in diabetic nephropathy and lupus nephritis and was stable throughout disease progression in acute transplant rejection and diabetic nephropathy; these results suggest renal VEGF-A splicing stability during kidney disease. The splicing patterns were species-specific; in the control human kidney samples, VEGF-A 121 was the dominant isoform, whereas VEGF-A 164 was the dominant isoform measured in the mouse kidney samples.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27598902</pmid><doi>10.1371/journal.pone.0162166</doi><tpages>e0162166</tpages><oa>free_for_read</oa></addata></record> |
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| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Alternative Splicing Analysis Angiogenesis Animal models Animals Autoimmune diseases Binding sites Biological activity Biology and Life Sciences Biopsy Case-Control Studies Control stability Diabetes Diabetes mellitus Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - metabolism Diabetes Mellitus, Type 2 - pathology Diabetes Mellitus, Type 2 - surgery Diabetic Nephropathies - genetics Diabetic Nephropathies - metabolism Diabetic Nephropathies - pathology Diabetic Nephropathies - surgery Diabetic nephropathy Disease control Disease Models, Animal Disease Progression Gene Expression Genetic aspects Graft rejection Graft Rejection - genetics Graft Rejection - immunology Graft Rejection - pathology Health aspects Humans Identification and classification Isoforms Kidney diseases Kidney Glomerulus - metabolism Kidney Glomerulus - pathology Kidney Transplantation Lupus Lupus nephritis Lupus Nephritis - genetics Lupus Nephritis - metabolism Lupus Nephritis - pathology Medicine and Health Sciences Mice mRNA Nephritis Nephropathy Pathology Patients Polymerase chain reaction Rejection Research and Analysis Methods Rodents Species Specificity Studies Transplantation Vascular endothelial growth factor Vascular Endothelial Growth Factor A - genetics Vascular Endothelial Growth Factor A - metabolism |
| title | Stability and Species Specificity of Renal VEGF-A Splicing Patterns in Kidney Disease |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-04T22%3A13%3A20IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Stability%20and%20Species%20Specificity%20of%20Renal%20VEGF-A%20Splicing%20Patterns%20in%20Kidney%20Disease&rft.jtitle=PloS%20one&rft.au=Turner,%20R%20J&rft.date=2016-09-06&rft.volume=11&rft.issue=9&rft.spage=e0162166&rft.epage=e0162166&rft.pages=e0162166-e0162166&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0162166&rft_dat=%3Cgale_plos_%3EA462656231%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1817110933&rft_id=info:pmid/27598902&rft_galeid=A462656231&rft_doaj_id=oai_doaj_org_article_77d6e97e11c344fdae9b75a4b37f8cc7&rfr_iscdi=true |