Upregulation of vascular endothelial growth factor isoform VEGF-164 and receptors (VEGFR-2, Npn-1, and Npn-2) in rats with cyclophosphamide-induced cystitis
Departments of 1 Neurology and 2 Anatomy, University of Vermont College of Medicine, Burlington, Vermont Submitted 13 May 2008 ; accepted in final form 11 July 2008 Regulation of the VEGF-VEGF receptor system was examined in the urinary bladder after acute (2–48 h) and chronic (10 days) cyclophospha...
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| Veröffentlicht in: | American Journal of Physiology - Renal Physiology 2008-09, Vol.295 (3), p.F826-F836 |
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| creator | Cheppudira, Bopaiah P Girard, Beatrice M Malley, Susan E Schutz, Kristin C May, Victor Vizzard, Margaret A |
| description | Departments of 1 Neurology and 2 Anatomy, University of Vermont College of Medicine, Burlington, Vermont
Submitted 13 May 2008
; accepted in final form 11 July 2008
Regulation of the VEGF-VEGF receptor system was examined in the urinary bladder after acute (2–48 h) and chronic (10 days) cyclophosphamide (CYP)-induced cystitis. ELISAs demonstrated significant ( P 0.01) upregulation of VEGF in whole urinary bladder with acute and chronic CYP-induced cystitis; however, the magnitude of increase was greater after acute (2–4 h) cystitis. Immunohistochemistry for VEGF immunoreactivity revealed a significant ( P 0.05) increase in VEGF immunoreactivity in the urothelium, suburothelial vasculature, and detrusor smooth muscle with acute (4 and 48 h) CYP treatment. RT-PCR identified the isoform VEGF-164, the VEGF receptor VEGFR-2, and the VEGF co-receptors neuropilin (Npn)-1 and Npn-2 in the urinary bladder. Quantitative PCR demonstrated upregulation of VEGF-164 transcript with acute and chronic CYP-induced cystitis, but VEGFR-2, Npn-1, and Npn-2 transcripts were upregulated ( P 0.01) in whole bladder only with chronic CYP-induced cystitis. Additional studies demonstrated regulation of VEGF transcript expression in the urinary bladder by nerve growth factor (NGF) in a novel line of NGF-overexpressing mice. These studies demonstrated that urinary bladder inflammation and NGF regulate the VEGF-VEGF receptor system in the urinary bladder. Functional role(s) for the VEGF-VEGF receptor system in urinary bladder inflammation remain to be determined.
urothelium; quantitative polymerase chain reaction; immunohistochemistry; detrusor smooth muscle; vasculature; nerve growth factor
Address for reprint requests and other correspondence: M. A. Vizzard, Dept. of Neurology, Univ. of Vermont College of Medicine, D415A Given Research Bldg., Burlington, VT 05405 (e-mail: margaret.vizzard{at}uvm.edu ) |
| doi_str_mv | 10.1152/ajprenal.90305.2008 |
| format | Article |
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Submitted 13 May 2008
; accepted in final form 11 July 2008
Regulation of the VEGF-VEGF receptor system was examined in the urinary bladder after acute (2–48 h) and chronic (10 days) cyclophosphamide (CYP)-induced cystitis. ELISAs demonstrated significant ( P 0.01) upregulation of VEGF in whole urinary bladder with acute and chronic CYP-induced cystitis; however, the magnitude of increase was greater after acute (2–4 h) cystitis. Immunohistochemistry for VEGF immunoreactivity revealed a significant ( P 0.05) increase in VEGF immunoreactivity in the urothelium, suburothelial vasculature, and detrusor smooth muscle with acute (4 and 48 h) CYP treatment. RT-PCR identified the isoform VEGF-164, the VEGF receptor VEGFR-2, and the VEGF co-receptors neuropilin (Npn)-1 and Npn-2 in the urinary bladder. Quantitative PCR demonstrated upregulation of VEGF-164 transcript with acute and chronic CYP-induced cystitis, but VEGFR-2, Npn-1, and Npn-2 transcripts were upregulated ( P 0.01) in whole bladder only with chronic CYP-induced cystitis. Additional studies demonstrated regulation of VEGF transcript expression in the urinary bladder by nerve growth factor (NGF) in a novel line of NGF-overexpressing mice. These studies demonstrated that urinary bladder inflammation and NGF regulate the VEGF-VEGF receptor system in the urinary bladder. Functional role(s) for the VEGF-VEGF receptor system in urinary bladder inflammation remain to be determined.
urothelium; quantitative polymerase chain reaction; immunohistochemistry; detrusor smooth muscle; vasculature; nerve growth factor
Address for reprint requests and other correspondence: M. A. Vizzard, Dept. of Neurology, Univ. of Vermont College of Medicine, D415A Given Research Bldg., Burlington, VT 05405 (e-mail: margaret.vizzard{at}uvm.edu )</description><identifier>ISSN: 0363-6127</identifier><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 2161-1157</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajprenal.90305.2008</identifier><identifier>PMID: 18632792</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Animals ; Antineoplastic Agents, Alkylating - pharmacology ; Bladder ; Cell growth ; Cells ; Cyclophosphamide - pharmacology ; Cystitis - chemically induced ; Cystitis - metabolism ; Enzyme-Linked Immunosorbent Assay ; Female ; Immunohistochemistry ; Membrane Proteins - genetics ; Muscle, Smooth - metabolism ; Nerve Growth Factor - metabolism ; Neuropilins - metabolism ; Promoter Regions, Genetic ; Protein Isoforms - metabolism ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism ; Rodents ; Up-Regulation ; Urinary Bladder - blood supply ; Urinary Bladder - drug effects ; Urinary Bladder - metabolism ; Urinary tract diseases ; Urogenital system ; Uroplakin II ; Urothelium - metabolism ; Vascular Endothelial Growth Factor A - metabolism ; Vascular Endothelial Growth Factor Receptor-2 - metabolism</subject><ispartof>American Journal of Physiology - Renal Physiology, 2008-09, Vol.295 (3), p.F826-F836</ispartof><rights>Copyright American Physiological Society Sep 2008</rights><rights>Copyright © 2008, American Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c520t-c47378937f62493ab41a5efdfd12f3ba7e347bfa68be13a38cd60909f60995ac3</citedby><cites>FETCH-LOGICAL-c520t-c47378937f62493ab41a5efdfd12f3ba7e347bfa68be13a38cd60909f60995ac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18632792$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cheppudira, Bopaiah P</creatorcontrib><creatorcontrib>Girard, Beatrice M</creatorcontrib><creatorcontrib>Malley, Susan E</creatorcontrib><creatorcontrib>Schutz, Kristin C</creatorcontrib><creatorcontrib>May, Victor</creatorcontrib><creatorcontrib>Vizzard, Margaret A</creatorcontrib><title>Upregulation of vascular endothelial growth factor isoform VEGF-164 and receptors (VEGFR-2, Npn-1, and Npn-2) in rats with cyclophosphamide-induced cystitis</title><title>American Journal of Physiology - Renal Physiology</title><addtitle>Am J Physiol Renal Physiol</addtitle><description>Departments of 1 Neurology and 2 Anatomy, University of Vermont College of Medicine, Burlington, Vermont
Submitted 13 May 2008
; accepted in final form 11 July 2008
Regulation of the VEGF-VEGF receptor system was examined in the urinary bladder after acute (2–48 h) and chronic (10 days) cyclophosphamide (CYP)-induced cystitis. ELISAs demonstrated significant ( P 0.01) upregulation of VEGF in whole urinary bladder with acute and chronic CYP-induced cystitis; however, the magnitude of increase was greater after acute (2–4 h) cystitis. Immunohistochemistry for VEGF immunoreactivity revealed a significant ( P 0.05) increase in VEGF immunoreactivity in the urothelium, suburothelial vasculature, and detrusor smooth muscle with acute (4 and 48 h) CYP treatment. RT-PCR identified the isoform VEGF-164, the VEGF receptor VEGFR-2, and the VEGF co-receptors neuropilin (Npn)-1 and Npn-2 in the urinary bladder. Quantitative PCR demonstrated upregulation of VEGF-164 transcript with acute and chronic CYP-induced cystitis, but VEGFR-2, Npn-1, and Npn-2 transcripts were upregulated ( P 0.01) in whole bladder only with chronic CYP-induced cystitis. Additional studies demonstrated regulation of VEGF transcript expression in the urinary bladder by nerve growth factor (NGF) in a novel line of NGF-overexpressing mice. These studies demonstrated that urinary bladder inflammation and NGF regulate the VEGF-VEGF receptor system in the urinary bladder. Functional role(s) for the VEGF-VEGF receptor system in urinary bladder inflammation remain to be determined.
urothelium; quantitative polymerase chain reaction; immunohistochemistry; detrusor smooth muscle; vasculature; nerve growth factor
Address for reprint requests and other correspondence: M. A. Vizzard, Dept. of Neurology, Univ. of Vermont College of Medicine, D415A Given Research Bldg., Burlington, VT 05405 (e-mail: margaret.vizzard{at}uvm.edu )</description><subject>Animals</subject><subject>Antineoplastic Agents, Alkylating - pharmacology</subject><subject>Bladder</subject><subject>Cell growth</subject><subject>Cells</subject><subject>Cyclophosphamide - pharmacology</subject><subject>Cystitis - chemically induced</subject><subject>Cystitis - metabolism</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Female</subject><subject>Immunohistochemistry</subject><subject>Membrane Proteins - genetics</subject><subject>Muscle, Smooth - metabolism</subject><subject>Nerve Growth Factor - metabolism</subject><subject>Neuropilins - metabolism</subject><subject>Promoter Regions, Genetic</subject><subject>Protein Isoforms - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Up-Regulation</subject><subject>Urinary Bladder - blood supply</subject><subject>Urinary Bladder - drug effects</subject><subject>Urinary Bladder - metabolism</subject><subject>Urinary tract diseases</subject><subject>Urogenital system</subject><subject>Uroplakin II</subject><subject>Urothelium - metabolism</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>Vascular Endothelial Growth Factor Receptor-2 - metabolism</subject><issn>0363-6127</issn><issn>1931-857X</issn><issn>2161-1157</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kVtv0zAcxS0EYt3gEyAhiycmLcWXxE54QELTOpAmkNDGq-X40rhK42A7K_0ufFjctXTwwItv55yf_9IB4BVGc4wr8k6uxmAG2c8bRFE1JwjVT8CMYIaLrPOnYIYoowXDhJ-A0xhXCBHCavYcnOCaUcIbMgO_7jJkOfUyOT9Ab-G9jCpfAzSD9qkzvZM9XAa_SR20UiUfoIve-rCG36-uFwVmJZSDhsEoM2Y1wre7928FuYBfxqHAFw_y7kjOoRtgkCnCjcs4tVW9Hzsfx06unTaFG_SkjM5CTC65-AI8s7KP5uVhPwN3i6vby0_Fzdfrz5cfbwpVEZQKVXLK64Zyy0jZUNmWWFbGaqsxsbSV3NCSt1ayujWYSlorzVCDGpvXppKKnoEPe-44tWujlRlSkL0Yg1vLsBVeOvGvMrhOLP29IBVlNa8z4M0BEPyPycQkVn4KuZsoCEUYc1ySbKJ7kwo-xmDs8QOMxK5R8adR8dCo2DWaU6__nu0xc6gwG97vDZ1bdhsXjBi7bXS-98utWEx9f2t-piOaNJWgYlETJkZtc3j-__BxnMcQ_Q0xJsaw</recordid><startdate>20080901</startdate><enddate>20080901</enddate><creator>Cheppudira, Bopaiah P</creator><creator>Girard, Beatrice M</creator><creator>Malley, Susan E</creator><creator>Schutz, Kristin C</creator><creator>May, Victor</creator><creator>Vizzard, Margaret A</creator><general>American Physiological Society</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>5PM</scope></search><sort><creationdate>20080901</creationdate><title>Upregulation of vascular endothelial growth factor isoform VEGF-164 and receptors (VEGFR-2, Npn-1, and Npn-2) in rats with cyclophosphamide-induced cystitis</title><author>Cheppudira, Bopaiah P ; Girard, Beatrice M ; Malley, Susan E ; Schutz, Kristin C ; May, Victor ; Vizzard, Margaret A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c520t-c47378937f62493ab41a5efdfd12f3ba7e347bfa68be13a38cd60909f60995ac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Antineoplastic Agents, Alkylating - pharmacology</topic><topic>Bladder</topic><topic>Cell growth</topic><topic>Cells</topic><topic>Cyclophosphamide - pharmacology</topic><topic>Cystitis - chemically induced</topic><topic>Cystitis - metabolism</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Female</topic><topic>Immunohistochemistry</topic><topic>Membrane Proteins - genetics</topic><topic>Muscle, Smooth - metabolism</topic><topic>Nerve Growth Factor - metabolism</topic><topic>Neuropilins - metabolism</topic><topic>Promoter Regions, Genetic</topic><topic>Protein Isoforms - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Up-Regulation</topic><topic>Urinary Bladder - blood supply</topic><topic>Urinary Bladder - drug effects</topic><topic>Urinary Bladder - metabolism</topic><topic>Urinary tract diseases</topic><topic>Urogenital system</topic><topic>Uroplakin II</topic><topic>Urothelium - metabolism</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>Vascular Endothelial Growth Factor Receptor-2 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheppudira, Bopaiah P</creatorcontrib><creatorcontrib>Girard, Beatrice M</creatorcontrib><creatorcontrib>Malley, Susan E</creatorcontrib><creatorcontrib>Schutz, Kristin C</creatorcontrib><creatorcontrib>May, Victor</creatorcontrib><creatorcontrib>Vizzard, Margaret A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American Journal of Physiology - Renal Physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheppudira, Bopaiah P</au><au>Girard, Beatrice M</au><au>Malley, Susan E</au><au>Schutz, Kristin C</au><au>May, Victor</au><au>Vizzard, Margaret A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of vascular endothelial growth factor isoform VEGF-164 and receptors (VEGFR-2, Npn-1, and Npn-2) in rats with cyclophosphamide-induced cystitis</atitle><jtitle>American Journal of Physiology - Renal Physiology</jtitle><addtitle>Am J Physiol Renal Physiol</addtitle><date>2008-09-01</date><risdate>2008</risdate><volume>295</volume><issue>3</issue><spage>F826</spage><epage>F836</epage><pages>F826-F836</pages><issn>0363-6127</issn><issn>1931-857X</issn><eissn>2161-1157</eissn><eissn>1522-1466</eissn><abstract>Departments of 1 Neurology and 2 Anatomy, University of Vermont College of Medicine, Burlington, Vermont
Submitted 13 May 2008
; accepted in final form 11 July 2008
Regulation of the VEGF-VEGF receptor system was examined in the urinary bladder after acute (2–48 h) and chronic (10 days) cyclophosphamide (CYP)-induced cystitis. ELISAs demonstrated significant ( P 0.01) upregulation of VEGF in whole urinary bladder with acute and chronic CYP-induced cystitis; however, the magnitude of increase was greater after acute (2–4 h) cystitis. Immunohistochemistry for VEGF immunoreactivity revealed a significant ( P 0.05) increase in VEGF immunoreactivity in the urothelium, suburothelial vasculature, and detrusor smooth muscle with acute (4 and 48 h) CYP treatment. RT-PCR identified the isoform VEGF-164, the VEGF receptor VEGFR-2, and the VEGF co-receptors neuropilin (Npn)-1 and Npn-2 in the urinary bladder. Quantitative PCR demonstrated upregulation of VEGF-164 transcript with acute and chronic CYP-induced cystitis, but VEGFR-2, Npn-1, and Npn-2 transcripts were upregulated ( P 0.01) in whole bladder only with chronic CYP-induced cystitis. Additional studies demonstrated regulation of VEGF transcript expression in the urinary bladder by nerve growth factor (NGF) in a novel line of NGF-overexpressing mice. These studies demonstrated that urinary bladder inflammation and NGF regulate the VEGF-VEGF receptor system in the urinary bladder. Functional role(s) for the VEGF-VEGF receptor system in urinary bladder inflammation remain to be determined.
urothelium; quantitative polymerase chain reaction; immunohistochemistry; detrusor smooth muscle; vasculature; nerve growth factor
Address for reprint requests and other correspondence: M. A. Vizzard, Dept. of Neurology, Univ. of Vermont College of Medicine, D415A Given Research Bldg., Burlington, VT 05405 (e-mail: margaret.vizzard{at}uvm.edu )</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>18632792</pmid><doi>10.1152/ajprenal.90305.2008</doi><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0363-6127 |
| ispartof | American Journal of Physiology - Renal Physiology, 2008-09, Vol.295 (3), p.F826-F836 |
| issn | 0363-6127 1931-857X 2161-1157 1522-1466 |
| language | eng |
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| source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Antineoplastic Agents, Alkylating - pharmacology Bladder Cell growth Cells Cyclophosphamide - pharmacology Cystitis - chemically induced Cystitis - metabolism Enzyme-Linked Immunosorbent Assay Female Immunohistochemistry Membrane Proteins - genetics Muscle, Smooth - metabolism Nerve Growth Factor - metabolism Neuropilins - metabolism Promoter Regions, Genetic Protein Isoforms - metabolism Rats Rats, Wistar Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism Rodents Up-Regulation Urinary Bladder - blood supply Urinary Bladder - drug effects Urinary Bladder - metabolism Urinary tract diseases Urogenital system Uroplakin II Urothelium - metabolism Vascular Endothelial Growth Factor A - metabolism Vascular Endothelial Growth Factor Receptor-2 - metabolism |
| title | Upregulation of vascular endothelial growth factor isoform VEGF-164 and receptors (VEGFR-2, Npn-1, and Npn-2) in rats with cyclophosphamide-induced cystitis |
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