High intestinal vascular permeability in a murine model for Hirschsprung’s disease: implications for postoperative Hirschsprung-associated enterocolitis
Purpose Intestinal vascular permeability (VP) in a murine model for Hirschsprung’s disease (HD) and postoperative Hirschsprung-associated enterocolitis (HAEC) were investigated. Methods Intestinal VP was determined using a Miles assay using 1% Evans blue injected into a superficial temporal vein of...
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| Veröffentlicht in: | Pediatric surgery international 2022-11, Vol.39 (1), p.15-15, Article 15 |
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| creator | Suda, Kazuto Yamada, Shunsuke Miyahara, Katsumi Fujiwara, Naho Kosaka, Seitaro Abe, Kumpei Seo, Shogo Nakamura, Shinji Lane, Geoffrey J. Yamataka, Atsuyuki |
| description | Purpose
Intestinal vascular permeability (VP) in a murine model for Hirschsprung’s disease (HD) and postoperative Hirschsprung-associated enterocolitis (HAEC) were investigated.
Methods
Intestinal VP was determined using a Miles assay using 1% Evans blue injected into a superficial temporal vein of newborn endothelin receptor-B KO HD model (KO) and syngeneic wild-type (WT) mice (
n
= 5, respectively). Extravasated Evans blue in normoganglionic ileum (Ng-I), normoganglionic proximal colon (Ng-PC) and aganglionic distal colon (Ag-DC) was quantified by absorbance at 620 nm. Quantitative polymerase chain reaction (qPCR) for Vascular Endothelial Growth Factor A (VEGF-A), VEGF-B, CDH5, SELE and CD31, and immunofluorescence for CD31 were performed.
Results
VP was significantly higher in Ng-I, Ng-PC, and Ag-DC from KO than WT (
p
|
| doi_str_mv | 10.1007/s00383-022-05308-7 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9713090</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2742879215</sourcerecordid><originalsourceid>FETCH-LOGICAL-c540t-e9103c168292df7f2ace6096b1fd9eb4d3650e50655d996ceeb70869e77ca33</originalsourceid><addsrcrecordid>eNp9kcFu1DAQhiMEoqXwAhyQJS5cAuM4tmMOSKgCFqkSB7hbjjPZdZXEwZOs1BuvAY_Hk2B2S2k5cLLl-eaf8f8XxVMOLzmAfkUAohElVFUJUkBT6nvFKa-FLk3Dxf1b95PiEdElADRCmYfFiVB1bTjnp8WPTdjuWJgWpCVMbmB7R34dXGIzphFdG4awXGWAOTauKUzIxtjhwPqY2CYk8jua0zptf377TqwLhI7wNQvjPATvlhAnOqBzpCVmyfy0xzuNpSOKPrgFO4Z5jxR9zDMDPS4e9G4gfHJ9nhWf37_7cr4pLz59-Hj-9qL0soalRMNBeK6aylRdr_vKeVRgVMv7zmBbd0JJQAlKys4Y5RFbDY0yqLV3QpwVb46q89qO2Pm8QnKDnVMYXbqy0QV7tzKFnd3GvTWaCzCQBV5cC6T4dc022jGQx2FwE8aVbKVrIUEaqTL6_B_0Mq4pu36gqkabistMVUfKp0iUsL9ZhoP9Hbw9Bm9z8PYQvNW56dntb9y0_Ek6A-IIZNfDtMX0d_Z_ZH8BQ4C_qg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2742879215</pqid></control><display><type>article</type><title>High intestinal vascular permeability in a murine model for Hirschsprung’s disease: implications for postoperative Hirschsprung-associated enterocolitis</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Suda, Kazuto ; Yamada, Shunsuke ; Miyahara, Katsumi ; Fujiwara, Naho ; Kosaka, Seitaro ; Abe, Kumpei ; Seo, Shogo ; Nakamura, Shinji ; Lane, Geoffrey J. ; Yamataka, Atsuyuki</creator><creatorcontrib>Suda, Kazuto ; Yamada, Shunsuke ; Miyahara, Katsumi ; Fujiwara, Naho ; Kosaka, Seitaro ; Abe, Kumpei ; Seo, Shogo ; Nakamura, Shinji ; Lane, Geoffrey J. ; Yamataka, Atsuyuki</creatorcontrib><description><![CDATA[Purpose
Intestinal vascular permeability (VP) in a murine model for Hirschsprung’s disease (HD) and postoperative Hirschsprung-associated enterocolitis (HAEC) were investigated.
Methods
Intestinal VP was determined using a Miles assay using 1% Evans blue injected into a superficial temporal vein of newborn endothelin receptor-B KO HD model (KO) and syngeneic wild-type (WT) mice (
n
= 5, respectively). Extravasated Evans blue in normoganglionic ileum (Ng-I), normoganglionic proximal colon (Ng-PC) and aganglionic distal colon (Ag-DC) was quantified by absorbance at 620 nm. Quantitative polymerase chain reaction (qPCR) for Vascular Endothelial Growth Factor A (VEGF-A), VEGF-B, CDH5, SELE and CD31, and immunofluorescence for CD31 were performed.
Results
VP was significantly higher in Ng-I, Ng-PC, and Ag-DC from KO than WT (
p
< 0.01,
p
< 0.05, and
p
< 0.05, respectively). qPCR demonstrated upregulated VEGF-A in Ng-I and Ag-DC, VEGF-B in Ng-I, and SELE in Ng-I and Ng-PC (
p
< 0.05,
p
< 0.05,
p
< 0.05,
p
< 0.01 and
p
< 0.05, respectively), and downregulated CDH5 in Ng-I and Ng-PC from KO (
p
< 0.05, respectively). Expression of CD31 mRNA in Ng-I and Ag-DC from KO was significantly higher on qPCR (
p
< 0.05) but differences on immunofluorescence were not significant.
Conclusions
VP may be etiologic for postoperative HAEC throughout the intestinal tract even after excision of aganglionic bowel.]]></description><identifier>ISSN: 1437-9813</identifier><identifier>ISSN: 0179-0358</identifier><identifier>EISSN: 1437-9813</identifier><identifier>DOI: 10.1007/s00383-022-05308-7</identifier><identifier>PMID: 36449111</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Angiogenesis ; Animals ; Antibodies ; Capillary Permeability ; Colon ; Disease ; Disease Models, Animal ; Enterocolitis - etiology ; Evans Blue ; Hirschsprung Disease - complications ; Laboratories ; Medicine ; Medicine & Public Health ; Mice ; Original ; Original Article ; Pediatric Surgery ; Pediatrics ; Permeability ; Polymerase chain reaction ; Postoperative period ; Rodents ; Small intestine ; Surgery ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - genetics ; Vascular Endothelial Growth Factor B</subject><ispartof>Pediatric surgery international, 2022-11, Vol.39 (1), p.15-15, Article 15</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c540t-e9103c168292df7f2ace6096b1fd9eb4d3650e50655d996ceeb70869e77ca33</citedby><cites>FETCH-LOGICAL-c540t-e9103c168292df7f2ace6096b1fd9eb4d3650e50655d996ceeb70869e77ca33</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/s00383-022-05308-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00383-022-05308-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36449111$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Suda, Kazuto</creatorcontrib><creatorcontrib>Yamada, Shunsuke</creatorcontrib><creatorcontrib>Miyahara, Katsumi</creatorcontrib><creatorcontrib>Fujiwara, Naho</creatorcontrib><creatorcontrib>Kosaka, Seitaro</creatorcontrib><creatorcontrib>Abe, Kumpei</creatorcontrib><creatorcontrib>Seo, Shogo</creatorcontrib><creatorcontrib>Nakamura, Shinji</creatorcontrib><creatorcontrib>Lane, Geoffrey J.</creatorcontrib><creatorcontrib>Yamataka, Atsuyuki</creatorcontrib><title>High intestinal vascular permeability in a murine model for Hirschsprung’s disease: implications for postoperative Hirschsprung-associated enterocolitis</title><title>Pediatric surgery international</title><addtitle>Pediatr Surg Int</addtitle><addtitle>Pediatr Surg Int</addtitle><description><![CDATA[Purpose
Intestinal vascular permeability (VP) in a murine model for Hirschsprung’s disease (HD) and postoperative Hirschsprung-associated enterocolitis (HAEC) were investigated.
Methods
Intestinal VP was determined using a Miles assay using 1% Evans blue injected into a superficial temporal vein of newborn endothelin receptor-B KO HD model (KO) and syngeneic wild-type (WT) mice (
n
= 5, respectively). Extravasated Evans blue in normoganglionic ileum (Ng-I), normoganglionic proximal colon (Ng-PC) and aganglionic distal colon (Ag-DC) was quantified by absorbance at 620 nm. Quantitative polymerase chain reaction (qPCR) for Vascular Endothelial Growth Factor A (VEGF-A), VEGF-B, CDH5, SELE and CD31, and immunofluorescence for CD31 were performed.
Results
VP was significantly higher in Ng-I, Ng-PC, and Ag-DC from KO than WT (
p
< 0.01,
p
< 0.05, and
p
< 0.05, respectively). qPCR demonstrated upregulated VEGF-A in Ng-I and Ag-DC, VEGF-B in Ng-I, and SELE in Ng-I and Ng-PC (
p
< 0.05,
p
< 0.05,
p
< 0.05,
p
< 0.01 and
p
< 0.05, respectively), and downregulated CDH5 in Ng-I and Ng-PC from KO (
p
< 0.05, respectively). Expression of CD31 mRNA in Ng-I and Ag-DC from KO was significantly higher on qPCR (
p
< 0.05) but differences on immunofluorescence were not significant.
Conclusions
VP may be etiologic for postoperative HAEC throughout the intestinal tract even after excision of aganglionic bowel.]]></description><subject>Angiogenesis</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Capillary Permeability</subject><subject>Colon</subject><subject>Disease</subject><subject>Disease Models, Animal</subject><subject>Enterocolitis - etiology</subject><subject>Evans Blue</subject><subject>Hirschsprung Disease - complications</subject><subject>Laboratories</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Original</subject><subject>Original Article</subject><subject>Pediatric Surgery</subject><subject>Pediatrics</subject><subject>Permeability</subject><subject>Polymerase chain reaction</subject><subject>Postoperative period</subject><subject>Rodents</subject><subject>Small intestine</subject><subject>Surgery</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - genetics</subject><subject>Vascular Endothelial Growth Factor B</subject><issn>1437-9813</issn><issn>0179-0358</issn><issn>1437-9813</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kcFu1DAQhiMEoqXwAhyQJS5cAuM4tmMOSKgCFqkSB7hbjjPZdZXEwZOs1BuvAY_Hk2B2S2k5cLLl-eaf8f8XxVMOLzmAfkUAohElVFUJUkBT6nvFKa-FLk3Dxf1b95PiEdElADRCmYfFiVB1bTjnp8WPTdjuWJgWpCVMbmB7R34dXGIzphFdG4awXGWAOTauKUzIxtjhwPqY2CYk8jua0zptf377TqwLhI7wNQvjPATvlhAnOqBzpCVmyfy0xzuNpSOKPrgFO4Z5jxR9zDMDPS4e9G4gfHJ9nhWf37_7cr4pLz59-Hj-9qL0soalRMNBeK6aylRdr_vKeVRgVMv7zmBbd0JJQAlKys4Y5RFbDY0yqLV3QpwVb46q89qO2Pm8QnKDnVMYXbqy0QV7tzKFnd3GvTWaCzCQBV5cC6T4dc022jGQx2FwE8aVbKVrIUEaqTL6_B_0Mq4pu36gqkabistMVUfKp0iUsL9ZhoP9Hbw9Bm9z8PYQvNW56dntb9y0_Ek6A-IIZNfDtMX0d_Z_ZH8BQ4C_qg</recordid><startdate>20221130</startdate><enddate>20221130</enddate><creator>Suda, Kazuto</creator><creator>Yamada, Shunsuke</creator><creator>Miyahara, Katsumi</creator><creator>Fujiwara, Naho</creator><creator>Kosaka, Seitaro</creator><creator>Abe, Kumpei</creator><creator>Seo, Shogo</creator><creator>Nakamura, Shinji</creator><creator>Lane, Geoffrey J.</creator><creator>Yamataka, Atsuyuki</creator><general>Springer Berlin Heidelberg</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>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>FYUFA</scope><scope>GHDGH</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20221130</creationdate><title>High intestinal vascular permeability in a murine model for Hirschsprung’s disease: implications for postoperative Hirschsprung-associated enterocolitis</title><author>Suda, Kazuto ; Yamada, Shunsuke ; Miyahara, Katsumi ; Fujiwara, Naho ; Kosaka, Seitaro ; Abe, Kumpei ; Seo, Shogo ; Nakamura, Shinji ; Lane, Geoffrey J. ; Yamataka, Atsuyuki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c540t-e9103c168292df7f2ace6096b1fd9eb4d3650e50655d996ceeb70869e77ca33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Angiogenesis</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Capillary Permeability</topic><topic>Colon</topic><topic>Disease</topic><topic>Disease Models, Animal</topic><topic>Enterocolitis - etiology</topic><topic>Evans Blue</topic><topic>Hirschsprung Disease - complications</topic><topic>Laboratories</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Original</topic><topic>Original Article</topic><topic>Pediatric Surgery</topic><topic>Pediatrics</topic><topic>Permeability</topic><topic>Polymerase chain reaction</topic><topic>Postoperative period</topic><topic>Rodents</topic><topic>Small intestine</topic><topic>Surgery</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - genetics</topic><topic>Vascular Endothelial Growth Factor B</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Suda, Kazuto</creatorcontrib><creatorcontrib>Yamada, Shunsuke</creatorcontrib><creatorcontrib>Miyahara, Katsumi</creatorcontrib><creatorcontrib>Fujiwara, Naho</creatorcontrib><creatorcontrib>Kosaka, Seitaro</creatorcontrib><creatorcontrib>Abe, Kumpei</creatorcontrib><creatorcontrib>Seo, Shogo</creatorcontrib><creatorcontrib>Nakamura, Shinji</creatorcontrib><creatorcontrib>Lane, Geoffrey J.</creatorcontrib><creatorcontrib>Yamataka, Atsuyuki</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>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Pediatric surgery international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Suda, Kazuto</au><au>Yamada, Shunsuke</au><au>Miyahara, Katsumi</au><au>Fujiwara, Naho</au><au>Kosaka, Seitaro</au><au>Abe, Kumpei</au><au>Seo, Shogo</au><au>Nakamura, Shinji</au><au>Lane, Geoffrey J.</au><au>Yamataka, Atsuyuki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High intestinal vascular permeability in a murine model for Hirschsprung’s disease: implications for postoperative Hirschsprung-associated enterocolitis</atitle><jtitle>Pediatric surgery international</jtitle><stitle>Pediatr Surg Int</stitle><addtitle>Pediatr Surg Int</addtitle><date>2022-11-30</date><risdate>2022</risdate><volume>39</volume><issue>1</issue><spage>15</spage><epage>15</epage><pages>15-15</pages><artnum>15</artnum><issn>1437-9813</issn><issn>0179-0358</issn><eissn>1437-9813</eissn><abstract><![CDATA[Purpose
Intestinal vascular permeability (VP) in a murine model for Hirschsprung’s disease (HD) and postoperative Hirschsprung-associated enterocolitis (HAEC) were investigated.
Methods
Intestinal VP was determined using a Miles assay using 1% Evans blue injected into a superficial temporal vein of newborn endothelin receptor-B KO HD model (KO) and syngeneic wild-type (WT) mice (
n
= 5, respectively). Extravasated Evans blue in normoganglionic ileum (Ng-I), normoganglionic proximal colon (Ng-PC) and aganglionic distal colon (Ag-DC) was quantified by absorbance at 620 nm. Quantitative polymerase chain reaction (qPCR) for Vascular Endothelial Growth Factor A (VEGF-A), VEGF-B, CDH5, SELE and CD31, and immunofluorescence for CD31 were performed.
Results
VP was significantly higher in Ng-I, Ng-PC, and Ag-DC from KO than WT (
p
< 0.01,
p
< 0.05, and
p
< 0.05, respectively). qPCR demonstrated upregulated VEGF-A in Ng-I and Ag-DC, VEGF-B in Ng-I, and SELE in Ng-I and Ng-PC (
p
< 0.05,
p
< 0.05,
p
< 0.05,
p
< 0.01 and
p
< 0.05, respectively), and downregulated CDH5 in Ng-I and Ng-PC from KO (
p
< 0.05, respectively). Expression of CD31 mRNA in Ng-I and Ag-DC from KO was significantly higher on qPCR (
p
< 0.05) but differences on immunofluorescence were not significant.
Conclusions
VP may be etiologic for postoperative HAEC throughout the intestinal tract even after excision of aganglionic bowel.]]></abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>36449111</pmid><doi>10.1007/s00383-022-05308-7</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1437-9813 |
| ispartof | Pediatric surgery international, 2022-11, Vol.39 (1), p.15-15, Article 15 |
| issn | 1437-9813 0179-0358 1437-9813 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9713090 |
| source | MEDLINE; SpringerLink Journals |
| subjects | Angiogenesis Animals Antibodies Capillary Permeability Colon Disease Disease Models, Animal Enterocolitis - etiology Evans Blue Hirschsprung Disease - complications Laboratories Medicine Medicine & Public Health Mice Original Original Article Pediatric Surgery Pediatrics Permeability Polymerase chain reaction Postoperative period Rodents Small intestine Surgery Vascular endothelial growth factor Vascular Endothelial Growth Factor A - genetics Vascular Endothelial Growth Factor B |
| title | High intestinal vascular permeability in a murine model for Hirschsprung’s disease: implications for postoperative Hirschsprung-associated enterocolitis |
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