Histopathological and proteomic analyses identify integrin-β1 as a potential mediator of phlebosclerosis in uremic patients
Background Patients with uremia have an excessive mortality from cardiovascular disease (CVD). Arterial remodeling is mainly responsible for uremia-induced CVD and has been well studied, yet venous remodeling is poorly understood. Here we investigate the histopathology and proteomic profiles of veno...
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| Veröffentlicht in: | Clinical and experimental nephrology 2019-09, Vol.23 (9), p.1100-1108 |
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| creator | Zhou, Chunyu Li, Changbin Wang, Qiang Wu, Mingyu Mohan, Chandra Hu, Dayong Peng, Ai |
| description | Background
Patients with uremia have an excessive mortality from cardiovascular disease (CVD). Arterial remodeling is mainly responsible for uremia-induced CVD and has been well studied, yet venous remodeling is poorly understood. Here we investigate the histopathology and proteomic profiles of venous remodeling in uremic patients.
Methods
Forearm cephalic veins were isolated from nine uremic patients during surgeries for arteriovenous fistula, and from nine healthy controls when applying surgical debridement. Hematoxylin–eosin, Masson’s trichrome, von Kossa, and immunohistochemistry (IHC) against proliferating cell nuclear antigen were stained for histopathology. Isobaric tags for relative and absolute quantitation (iTRAQ) proteomic analysis was executed to explore the proteome of the veins. The core regulatory protein was validated by western blot, IHC, and immunofluorescence.
Results
Phlebosclerosis, characterized by intimal rarefaction and medial thickening with disordered proliferation of vascular smooth muscle cells (VSMCs), was the prominent pathological manifestation of peripheral veins in uremic patients, while inflammatory cell infiltration, atherosclerosis or calcification were not obviously detected. iTRAQ analysis showed that 350 proteins were significantly changed in phlebosclerosis of uremic patients compared with healthy controls, of which integrin-β1 (ITGβ1) exhibited the strongest regulatory ability by intermolecular interaction network analysis. The enhanced ITGβ1 expression was mainly co-expressed with the disordered proliferation of VSMCs while a little with vascular endothelial cells in the forearm cephalic veins of uremic patients.
Conclusions
Phlebosclerosis is the prominent pathological manifestation in peripheral veins of uremic patients. This pathological alteration mainly attributes to the disordered proliferation of VSMCs, which is potentially mediated by ITGβ1. |
| doi_str_mv | 10.1007/s10157-019-01755-0 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2243491425</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2242645404</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3690-ae10db3cf8ea803676119c520a6242a1ecb86639de5f6cd48231d6e4692756ac3</originalsourceid><addsrcrecordid>eNp9kc9KHTEUxkNR1Kov0EUJdONmav5nsiyiVRC6qeuQmzlzjcydTJOZxYU-lQ_iM_XotS24cBGScH7fdzjnI-QTZ185Y_a8csa1bRh3eKzWDftAjriStrHWuT18SyUarPBD8rHWB8ZY67Q7IIeSC65aK47I7-tU5zyF-T4PeZ1iGGgYOzqVPEPepIi_MGwrVJo6GOfUb2kaZ1iXNDZPj5yGSgOdEMYaajfQpTDnQnNPp_sBVrnGAUquCQ1GuhR49sR2CQX1hOz3Yahw-nofk7ury58X183tj-83F99umyiNY00AzrqVjH0LoWXSWMO5i1qwYIQSgUNctcZI14HuTexUKyTvDCjjhNUmRHlMzna-ONavBersN6lGGIYwQl6qF0JJ5bgSGtEvb9CHvBTcwQsljNKKKaTEjoo4Wi3Q-6mkTShbz5l_zsbvsvGYjX_JxjMUfX61Xla4p3-Sv2EgIHdAxdK4hvK_9zu2fwAzFZvb</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2242645404</pqid></control><display><type>article</type><title>Histopathological and proteomic analyses identify integrin-β1 as a potential mediator of phlebosclerosis in uremic patients</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Zhou, Chunyu ; Li, Changbin ; Wang, Qiang ; Wu, Mingyu ; Mohan, Chandra ; Hu, Dayong ; Peng, Ai</creator><creatorcontrib>Zhou, Chunyu ; Li, Changbin ; Wang, Qiang ; Wu, Mingyu ; Mohan, Chandra ; Hu, Dayong ; Peng, Ai</creatorcontrib><description>Background
Patients with uremia have an excessive mortality from cardiovascular disease (CVD). Arterial remodeling is mainly responsible for uremia-induced CVD and has been well studied, yet venous remodeling is poorly understood. Here we investigate the histopathology and proteomic profiles of venous remodeling in uremic patients.
Methods
Forearm cephalic veins were isolated from nine uremic patients during surgeries for arteriovenous fistula, and from nine healthy controls when applying surgical debridement. Hematoxylin–eosin, Masson’s trichrome, von Kossa, and immunohistochemistry (IHC) against proliferating cell nuclear antigen were stained for histopathology. Isobaric tags for relative and absolute quantitation (iTRAQ) proteomic analysis was executed to explore the proteome of the veins. The core regulatory protein was validated by western blot, IHC, and immunofluorescence.
Results
Phlebosclerosis, characterized by intimal rarefaction and medial thickening with disordered proliferation of vascular smooth muscle cells (VSMCs), was the prominent pathological manifestation of peripheral veins in uremic patients, while inflammatory cell infiltration, atherosclerosis or calcification were not obviously detected. iTRAQ analysis showed that 350 proteins were significantly changed in phlebosclerosis of uremic patients compared with healthy controls, of which integrin-β1 (ITGβ1) exhibited the strongest regulatory ability by intermolecular interaction network analysis. The enhanced ITGβ1 expression was mainly co-expressed with the disordered proliferation of VSMCs while a little with vascular endothelial cells in the forearm cephalic veins of uremic patients.
Conclusions
Phlebosclerosis is the prominent pathological manifestation in peripheral veins of uremic patients. This pathological alteration mainly attributes to the disordered proliferation of VSMCs, which is potentially mediated by ITGβ1.</description><identifier>ISSN: 1342-1751</identifier><identifier>EISSN: 1437-7799</identifier><identifier>DOI: 10.1007/s10157-019-01755-0</identifier><identifier>PMID: 31214872</identifier><language>eng</language><publisher>Singapore: Springer Singapore</publisher><subject>Arteriosclerosis ; Calcification (ectopic) ; Cardiovascular diseases ; Case-Control Studies ; Cell Proliferation ; Endothelial cells ; Endothelial Cells - chemistry ; Endothelial Cells - pathology ; Female ; Fistulae ; Forearm ; Forearm - blood supply ; Histopathology ; Humans ; Immunofluorescence ; Immunohistochemistry ; Inflammation ; Integrin beta1 - analysis ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Muscle, Smooth, Vascular - chemistry ; Muscle, Smooth, Vascular - pathology ; Myocytes, Smooth Muscle - chemistry ; Myocytes, Smooth Muscle - pathology ; Nephrology ; Original Article ; Peripheral Vascular Diseases - etiology ; Peripheral Vascular Diseases - metabolism ; Peripheral Vascular Diseases - pathology ; Proliferating cell nuclear antigen ; Proteomes ; Proteomics - methods ; Quantitation ; Sclerosis ; Smooth muscle ; Uremia ; Uremia - complications ; Uremia - diagnosis ; Urology ; Vascular Remodeling ; Veins & arteries ; Veins - chemistry ; Veins - pathology</subject><ispartof>Clinical and experimental nephrology, 2019-09, Vol.23 (9), p.1100-1108</ispartof><rights>Japanese Society of Nephrology 2019</rights><rights>Clinical and Experimental Nephrology is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3690-ae10db3cf8ea803676119c520a6242a1ecb86639de5f6cd48231d6e4692756ac3</citedby><cites>FETCH-LOGICAL-c3690-ae10db3cf8ea803676119c520a6242a1ecb86639de5f6cd48231d6e4692756ac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10157-019-01755-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10157-019-01755-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31214872$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Chunyu</creatorcontrib><creatorcontrib>Li, Changbin</creatorcontrib><creatorcontrib>Wang, Qiang</creatorcontrib><creatorcontrib>Wu, Mingyu</creatorcontrib><creatorcontrib>Mohan, Chandra</creatorcontrib><creatorcontrib>Hu, Dayong</creatorcontrib><creatorcontrib>Peng, Ai</creatorcontrib><title>Histopathological and proteomic analyses identify integrin-β1 as a potential mediator of phlebosclerosis in uremic patients</title><title>Clinical and experimental nephrology</title><addtitle>Clin Exp Nephrol</addtitle><addtitle>Clin Exp Nephrol</addtitle><description>Background
Patients with uremia have an excessive mortality from cardiovascular disease (CVD). Arterial remodeling is mainly responsible for uremia-induced CVD and has been well studied, yet venous remodeling is poorly understood. Here we investigate the histopathology and proteomic profiles of venous remodeling in uremic patients.
Methods
Forearm cephalic veins were isolated from nine uremic patients during surgeries for arteriovenous fistula, and from nine healthy controls when applying surgical debridement. Hematoxylin–eosin, Masson’s trichrome, von Kossa, and immunohistochemistry (IHC) against proliferating cell nuclear antigen were stained for histopathology. Isobaric tags for relative and absolute quantitation (iTRAQ) proteomic analysis was executed to explore the proteome of the veins. The core regulatory protein was validated by western blot, IHC, and immunofluorescence.
Results
Phlebosclerosis, characterized by intimal rarefaction and medial thickening with disordered proliferation of vascular smooth muscle cells (VSMCs), was the prominent pathological manifestation of peripheral veins in uremic patients, while inflammatory cell infiltration, atherosclerosis or calcification were not obviously detected. iTRAQ analysis showed that 350 proteins were significantly changed in phlebosclerosis of uremic patients compared with healthy controls, of which integrin-β1 (ITGβ1) exhibited the strongest regulatory ability by intermolecular interaction network analysis. The enhanced ITGβ1 expression was mainly co-expressed with the disordered proliferation of VSMCs while a little with vascular endothelial cells in the forearm cephalic veins of uremic patients.
Conclusions
Phlebosclerosis is the prominent pathological manifestation in peripheral veins of uremic patients. This pathological alteration mainly attributes to the disordered proliferation of VSMCs, which is potentially mediated by ITGβ1.</description><subject>Arteriosclerosis</subject><subject>Calcification (ectopic)</subject><subject>Cardiovascular diseases</subject><subject>Case-Control Studies</subject><subject>Cell Proliferation</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - chemistry</subject><subject>Endothelial Cells - pathology</subject><subject>Female</subject><subject>Fistulae</subject><subject>Forearm</subject><subject>Forearm - blood supply</subject><subject>Histopathology</subject><subject>Humans</subject><subject>Immunofluorescence</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Integrin beta1 - analysis</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Muscle, Smooth, Vascular - chemistry</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>Myocytes, Smooth Muscle - chemistry</subject><subject>Myocytes, Smooth Muscle - pathology</subject><subject>Nephrology</subject><subject>Original Article</subject><subject>Peripheral Vascular Diseases - etiology</subject><subject>Peripheral Vascular Diseases - metabolism</subject><subject>Peripheral Vascular Diseases - pathology</subject><subject>Proliferating cell nuclear antigen</subject><subject>Proteomes</subject><subject>Proteomics - methods</subject><subject>Quantitation</subject><subject>Sclerosis</subject><subject>Smooth muscle</subject><subject>Uremia</subject><subject>Uremia - complications</subject><subject>Uremia - diagnosis</subject><subject>Urology</subject><subject>Vascular Remodeling</subject><subject>Veins & arteries</subject><subject>Veins - chemistry</subject><subject>Veins - pathology</subject><issn>1342-1751</issn><issn>1437-7799</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kc9KHTEUxkNR1Kov0EUJdONmav5nsiyiVRC6qeuQmzlzjcydTJOZxYU-lQ_iM_XotS24cBGScH7fdzjnI-QTZ185Y_a8csa1bRh3eKzWDftAjriStrHWuT18SyUarPBD8rHWB8ZY67Q7IIeSC65aK47I7-tU5zyF-T4PeZ1iGGgYOzqVPEPepIi_MGwrVJo6GOfUb2kaZ1iXNDZPj5yGSgOdEMYaajfQpTDnQnNPp_sBVrnGAUquCQ1GuhR49sR2CQX1hOz3Yahw-nofk7ury58X183tj-83F99umyiNY00AzrqVjH0LoWXSWMO5i1qwYIQSgUNctcZI14HuTexUKyTvDCjjhNUmRHlMzna-ONavBersN6lGGIYwQl6qF0JJ5bgSGtEvb9CHvBTcwQsljNKKKaTEjoo4Wi3Q-6mkTShbz5l_zsbvsvGYjX_JxjMUfX61Xla4p3-Sv2EgIHdAxdK4hvK_9zu2fwAzFZvb</recordid><startdate>20190901</startdate><enddate>20190901</enddate><creator>Zhou, Chunyu</creator><creator>Li, Changbin</creator><creator>Wang, Qiang</creator><creator>Wu, Mingyu</creator><creator>Mohan, Chandra</creator><creator>Hu, Dayong</creator><creator>Peng, Ai</creator><general>Springer Singapore</general><general>Springer Nature B.V</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>7QP</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20190901</creationdate><title>Histopathological and proteomic analyses identify integrin-β1 as a potential mediator of phlebosclerosis in uremic patients</title><author>Zhou, Chunyu ; Li, Changbin ; Wang, Qiang ; Wu, Mingyu ; Mohan, Chandra ; Hu, Dayong ; Peng, Ai</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3690-ae10db3cf8ea803676119c520a6242a1ecb86639de5f6cd48231d6e4692756ac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Arteriosclerosis</topic><topic>Calcification (ectopic)</topic><topic>Cardiovascular diseases</topic><topic>Case-Control Studies</topic><topic>Cell Proliferation</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - chemistry</topic><topic>Endothelial Cells - pathology</topic><topic>Female</topic><topic>Fistulae</topic><topic>Forearm</topic><topic>Forearm - blood supply</topic><topic>Histopathology</topic><topic>Humans</topic><topic>Immunofluorescence</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Integrin beta1 - analysis</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Muscle, Smooth, Vascular - chemistry</topic><topic>Muscle, Smooth, Vascular - pathology</topic><topic>Myocytes, Smooth Muscle - chemistry</topic><topic>Myocytes, Smooth Muscle - pathology</topic><topic>Nephrology</topic><topic>Original Article</topic><topic>Peripheral Vascular Diseases - etiology</topic><topic>Peripheral Vascular Diseases - metabolism</topic><topic>Peripheral Vascular Diseases - pathology</topic><topic>Proliferating cell nuclear antigen</topic><topic>Proteomes</topic><topic>Proteomics - methods</topic><topic>Quantitation</topic><topic>Sclerosis</topic><topic>Smooth muscle</topic><topic>Uremia</topic><topic>Uremia - complications</topic><topic>Uremia - diagnosis</topic><topic>Urology</topic><topic>Vascular Remodeling</topic><topic>Veins & arteries</topic><topic>Veins - chemistry</topic><topic>Veins - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Chunyu</creatorcontrib><creatorcontrib>Li, Changbin</creatorcontrib><creatorcontrib>Wang, Qiang</creatorcontrib><creatorcontrib>Wu, Mingyu</creatorcontrib><creatorcontrib>Mohan, Chandra</creatorcontrib><creatorcontrib>Hu, Dayong</creatorcontrib><creatorcontrib>Peng, Ai</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>Calcium & Calcified Tissue Abstracts</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>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</collection><collection>ProQuest One Community College</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>Medical 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><jtitle>Clinical and experimental nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Chunyu</au><au>Li, Changbin</au><au>Wang, Qiang</au><au>Wu, Mingyu</au><au>Mohan, Chandra</au><au>Hu, Dayong</au><au>Peng, Ai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Histopathological and proteomic analyses identify integrin-β1 as a potential mediator of phlebosclerosis in uremic patients</atitle><jtitle>Clinical and experimental nephrology</jtitle><stitle>Clin Exp Nephrol</stitle><addtitle>Clin Exp Nephrol</addtitle><date>2019-09-01</date><risdate>2019</risdate><volume>23</volume><issue>9</issue><spage>1100</spage><epage>1108</epage><pages>1100-1108</pages><issn>1342-1751</issn><eissn>1437-7799</eissn><abstract>Background
Patients with uremia have an excessive mortality from cardiovascular disease (CVD). Arterial remodeling is mainly responsible for uremia-induced CVD and has been well studied, yet venous remodeling is poorly understood. Here we investigate the histopathology and proteomic profiles of venous remodeling in uremic patients.
Methods
Forearm cephalic veins were isolated from nine uremic patients during surgeries for arteriovenous fistula, and from nine healthy controls when applying surgical debridement. Hematoxylin–eosin, Masson’s trichrome, von Kossa, and immunohistochemistry (IHC) against proliferating cell nuclear antigen were stained for histopathology. Isobaric tags for relative and absolute quantitation (iTRAQ) proteomic analysis was executed to explore the proteome of the veins. The core regulatory protein was validated by western blot, IHC, and immunofluorescence.
Results
Phlebosclerosis, characterized by intimal rarefaction and medial thickening with disordered proliferation of vascular smooth muscle cells (VSMCs), was the prominent pathological manifestation of peripheral veins in uremic patients, while inflammatory cell infiltration, atherosclerosis or calcification were not obviously detected. iTRAQ analysis showed that 350 proteins were significantly changed in phlebosclerosis of uremic patients compared with healthy controls, of which integrin-β1 (ITGβ1) exhibited the strongest regulatory ability by intermolecular interaction network analysis. The enhanced ITGβ1 expression was mainly co-expressed with the disordered proliferation of VSMCs while a little with vascular endothelial cells in the forearm cephalic veins of uremic patients.
Conclusions
Phlebosclerosis is the prominent pathological manifestation in peripheral veins of uremic patients. This pathological alteration mainly attributes to the disordered proliferation of VSMCs, which is potentially mediated by ITGβ1.</abstract><cop>Singapore</cop><pub>Springer Singapore</pub><pmid>31214872</pmid><doi>10.1007/s10157-019-01755-0</doi><tpages>9</tpages></addata></record> |
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| subjects | Arteriosclerosis Calcification (ectopic) Cardiovascular diseases Case-Control Studies Cell Proliferation Endothelial cells Endothelial Cells - chemistry Endothelial Cells - pathology Female Fistulae Forearm Forearm - blood supply Histopathology Humans Immunofluorescence Immunohistochemistry Inflammation Integrin beta1 - analysis Male Medicine Medicine & Public Health Middle Aged Muscle, Smooth, Vascular - chemistry Muscle, Smooth, Vascular - pathology Myocytes, Smooth Muscle - chemistry Myocytes, Smooth Muscle - pathology Nephrology Original Article Peripheral Vascular Diseases - etiology Peripheral Vascular Diseases - metabolism Peripheral Vascular Diseases - pathology Proliferating cell nuclear antigen Proteomes Proteomics - methods Quantitation Sclerosis Smooth muscle Uremia Uremia - complications Uremia - diagnosis Urology Vascular Remodeling Veins & arteries Veins - chemistry Veins - pathology |
| title | Histopathological and proteomic analyses identify integrin-β1 as a potential mediator of phlebosclerosis in uremic patients |
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