Myocardial fibrosis after adrenergic stimulation as a long-term sequela in a mouse model of Kawasaki disease vasculitis

Kawasaki disease (KD), the leading cause of acquired cardiac disease among children, is often associated with myocarditis that may lead to long-term myocardial dysfunction and fibrosis. Although those myocardial changes develop during the acute phase, they may persist for decades and closely correla...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:JCI insight 2019-02, Vol.4 (3)
Hauptverfasser: Matundan, Harry H, Sin, Jon, Rivas, Magali Noval, Fishbein, Michael C, Lehman, Thomas J, Chen, Shuang, Gottlieb, Roberta A, Crother, Timothy R, Abe, Masanori, Arditi, Moshe
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page
container_issue 3
container_start_page
container_title JCI insight
container_volume 4
creator Matundan, Harry H
Sin, Jon
Rivas, Magali Noval
Fishbein, Michael C
Lehman, Thomas J
Chen, Shuang
Gottlieb, Roberta A
Crother, Timothy R
Abe, Masanori
Arditi, Moshe
description Kawasaki disease (KD), the leading cause of acquired cardiac disease among children, is often associated with myocarditis that may lead to long-term myocardial dysfunction and fibrosis. Although those myocardial changes develop during the acute phase, they may persist for decades and closely correlate with long-term myocardial sequelae. Using the Lactobacillus casei cell wall extract-induced (LCWE-induced) KD vasculitis murine model, we investigated long-term cardiovascular sequelae, such as myocardial dysfunction, fibrosis, and coronary microvascular lesions following adrenergic stimuli after established KD vasculitis. We found that adrenergic stimulation with isoproterenol following LCWE-induced KD vasculitis in mice was associated with increased risk of cardiac hypertrophy and myocardial fibrosis, diminished ejection fraction, and increased serum levels of brain natriuretic peptide. Myocardial fibrosis resulting from pharmacologic-induced exercise after KD development was IL-1 signaling dependent and was associated with a significant reduction in myocardial capillary CD31 expression, indicative of a rarefied myocardial capillary bed. These observations suggest that adrenergic stimulation after KD vasculitis may lead to cardiac hypertrophy and bridging fibrosis in the myocardium in the LCWE-induced KD vasculitis mouse model and that this process involves IL-1 signaling and diminished microvascular circulation in the myocardium.
doi_str_mv 10.1172/jci.insight.126279
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6413776</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2204684107</sourcerecordid><originalsourceid>FETCH-LOGICAL-c468t-524ccfedb6f047d712f762081967f69af2f9d7efdd32a268aab000288ad4c6483</originalsourceid><addsrcrecordid>eNpVUctuFDEQtBCIRCE_wAH5yGU2ds_E9lyQUEQAJYgLnK1ePzYdPONgzyTK32O0SxQubktVXd3VxdhbKTZSaji7dbShudLuZtlIUKDHF-wYej12vRbm5bP_ETut9VYIIfUA4ty8Zke90GB6GI_Zw7fH7LB4wsQjbUuuVDnGJRSOvoQ5lB05Xhea1oQL5Zljw3nK865rpInX8HsNCTk1hE95raG9PiSeI7_CB6z4i7inGrAh91jdmmih-oa9iphqOD3UE_bz8tOPiy_d9ffPXy8-XnduUGbpzmFwLga_VVEM2msJUSsQRo5KRzVihDh6HaL3PSAog7htRsEY9INTg-lP2Ie97t26nYJ3YV4KJntXaMLyaDOS_R-Z6cbu8r1Vg-y1Vk3g_UGg5Oa0Lnai6kJKOIfm1gKItukghW5U2FNdO2MtIT6NkcL-Dc220OwhNLsPrTW9e77gU8u_iPo_knOZWg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2204684107</pqid></control><display><type>article</type><title>Myocardial fibrosis after adrenergic stimulation as a long-term sequela in a mouse model of Kawasaki disease vasculitis</title><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Matundan, Harry H ; Sin, Jon ; Rivas, Magali Noval ; Fishbein, Michael C ; Lehman, Thomas J ; Chen, Shuang ; Gottlieb, Roberta A ; Crother, Timothy R ; Abe, Masanori ; Arditi, Moshe</creator><creatorcontrib>Matundan, Harry H ; Sin, Jon ; Rivas, Magali Noval ; Fishbein, Michael C ; Lehman, Thomas J ; Chen, Shuang ; Gottlieb, Roberta A ; Crother, Timothy R ; Abe, Masanori ; Arditi, Moshe</creatorcontrib><description>Kawasaki disease (KD), the leading cause of acquired cardiac disease among children, is often associated with myocarditis that may lead to long-term myocardial dysfunction and fibrosis. Although those myocardial changes develop during the acute phase, they may persist for decades and closely correlate with long-term myocardial sequelae. Using the Lactobacillus casei cell wall extract-induced (LCWE-induced) KD vasculitis murine model, we investigated long-term cardiovascular sequelae, such as myocardial dysfunction, fibrosis, and coronary microvascular lesions following adrenergic stimuli after established KD vasculitis. We found that adrenergic stimulation with isoproterenol following LCWE-induced KD vasculitis in mice was associated with increased risk of cardiac hypertrophy and myocardial fibrosis, diminished ejection fraction, and increased serum levels of brain natriuretic peptide. Myocardial fibrosis resulting from pharmacologic-induced exercise after KD development was IL-1 signaling dependent and was associated with a significant reduction in myocardial capillary CD31 expression, indicative of a rarefied myocardial capillary bed. These observations suggest that adrenergic stimulation after KD vasculitis may lead to cardiac hypertrophy and bridging fibrosis in the myocardium in the LCWE-induced KD vasculitis mouse model and that this process involves IL-1 signaling and diminished microvascular circulation in the myocardium.</description><identifier>ISSN: 2379-3708</identifier><identifier>EISSN: 2379-3708</identifier><identifier>DOI: 10.1172/jci.insight.126279</identifier><identifier>PMID: 30728329</identifier><language>eng</language><publisher>United States: American Society for Clinical Investigation</publisher><ispartof>JCI insight, 2019-02, Vol.4 (3)</ispartof><rights>Copyright © 2019, American Society for Clinical Investigation 2019 American Society for Clinical Investigation</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-524ccfedb6f047d712f762081967f69af2f9d7efdd32a268aab000288ad4c6483</citedby><cites>FETCH-LOGICAL-c468t-524ccfedb6f047d712f762081967f69af2f9d7efdd32a268aab000288ad4c6483</cites><orcidid>0000-0002-1432-006X ; 0000-0001-5570-8928</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6413776/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6413776/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30728329$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matundan, Harry H</creatorcontrib><creatorcontrib>Sin, Jon</creatorcontrib><creatorcontrib>Rivas, Magali Noval</creatorcontrib><creatorcontrib>Fishbein, Michael C</creatorcontrib><creatorcontrib>Lehman, Thomas J</creatorcontrib><creatorcontrib>Chen, Shuang</creatorcontrib><creatorcontrib>Gottlieb, Roberta A</creatorcontrib><creatorcontrib>Crother, Timothy R</creatorcontrib><creatorcontrib>Abe, Masanori</creatorcontrib><creatorcontrib>Arditi, Moshe</creatorcontrib><title>Myocardial fibrosis after adrenergic stimulation as a long-term sequela in a mouse model of Kawasaki disease vasculitis</title><title>JCI insight</title><addtitle>JCI Insight</addtitle><description>Kawasaki disease (KD), the leading cause of acquired cardiac disease among children, is often associated with myocarditis that may lead to long-term myocardial dysfunction and fibrosis. Although those myocardial changes develop during the acute phase, they may persist for decades and closely correlate with long-term myocardial sequelae. Using the Lactobacillus casei cell wall extract-induced (LCWE-induced) KD vasculitis murine model, we investigated long-term cardiovascular sequelae, such as myocardial dysfunction, fibrosis, and coronary microvascular lesions following adrenergic stimuli after established KD vasculitis. We found that adrenergic stimulation with isoproterenol following LCWE-induced KD vasculitis in mice was associated with increased risk of cardiac hypertrophy and myocardial fibrosis, diminished ejection fraction, and increased serum levels of brain natriuretic peptide. Myocardial fibrosis resulting from pharmacologic-induced exercise after KD development was IL-1 signaling dependent and was associated with a significant reduction in myocardial capillary CD31 expression, indicative of a rarefied myocardial capillary bed. These observations suggest that adrenergic stimulation after KD vasculitis may lead to cardiac hypertrophy and bridging fibrosis in the myocardium in the LCWE-induced KD vasculitis mouse model and that this process involves IL-1 signaling and diminished microvascular circulation in the myocardium.</description><issn>2379-3708</issn><issn>2379-3708</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNpVUctuFDEQtBCIRCE_wAH5yGU2ds_E9lyQUEQAJYgLnK1ePzYdPONgzyTK32O0SxQubktVXd3VxdhbKTZSaji7dbShudLuZtlIUKDHF-wYej12vRbm5bP_ETut9VYIIfUA4ty8Zke90GB6GI_Zw7fH7LB4wsQjbUuuVDnGJRSOvoQ5lB05Xhea1oQL5Zljw3nK865rpInX8HsNCTk1hE95raG9PiSeI7_CB6z4i7inGrAh91jdmmih-oa9iphqOD3UE_bz8tOPiy_d9ffPXy8-XnduUGbpzmFwLga_VVEM2msJUSsQRo5KRzVihDh6HaL3PSAog7htRsEY9INTg-lP2Ie97t26nYJ3YV4KJntXaMLyaDOS_R-Z6cbu8r1Vg-y1Vk3g_UGg5Oa0Lnai6kJKOIfm1gKItukghW5U2FNdO2MtIT6NkcL-Dc220OwhNLsPrTW9e77gU8u_iPo_knOZWg</recordid><startdate>20190207</startdate><enddate>20190207</enddate><creator>Matundan, Harry H</creator><creator>Sin, Jon</creator><creator>Rivas, Magali Noval</creator><creator>Fishbein, Michael C</creator><creator>Lehman, Thomas J</creator><creator>Chen, Shuang</creator><creator>Gottlieb, Roberta A</creator><creator>Crother, Timothy R</creator><creator>Abe, Masanori</creator><creator>Arditi, Moshe</creator><general>American Society for Clinical Investigation</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1432-006X</orcidid><orcidid>https://orcid.org/0000-0001-5570-8928</orcidid></search><sort><creationdate>20190207</creationdate><title>Myocardial fibrosis after adrenergic stimulation as a long-term sequela in a mouse model of Kawasaki disease vasculitis</title><author>Matundan, Harry H ; Sin, Jon ; Rivas, Magali Noval ; Fishbein, Michael C ; Lehman, Thomas J ; Chen, Shuang ; Gottlieb, Roberta A ; Crother, Timothy R ; Abe, Masanori ; Arditi, Moshe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-524ccfedb6f047d712f762081967f69af2f9d7efdd32a268aab000288ad4c6483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matundan, Harry H</creatorcontrib><creatorcontrib>Sin, Jon</creatorcontrib><creatorcontrib>Rivas, Magali Noval</creatorcontrib><creatorcontrib>Fishbein, Michael C</creatorcontrib><creatorcontrib>Lehman, Thomas J</creatorcontrib><creatorcontrib>Chen, Shuang</creatorcontrib><creatorcontrib>Gottlieb, Roberta A</creatorcontrib><creatorcontrib>Crother, Timothy R</creatorcontrib><creatorcontrib>Abe, Masanori</creatorcontrib><creatorcontrib>Arditi, Moshe</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>JCI insight</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matundan, Harry H</au><au>Sin, Jon</au><au>Rivas, Magali Noval</au><au>Fishbein, Michael C</au><au>Lehman, Thomas J</au><au>Chen, Shuang</au><au>Gottlieb, Roberta A</au><au>Crother, Timothy R</au><au>Abe, Masanori</au><au>Arditi, Moshe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myocardial fibrosis after adrenergic stimulation as a long-term sequela in a mouse model of Kawasaki disease vasculitis</atitle><jtitle>JCI insight</jtitle><addtitle>JCI Insight</addtitle><date>2019-02-07</date><risdate>2019</risdate><volume>4</volume><issue>3</issue><issn>2379-3708</issn><eissn>2379-3708</eissn><abstract>Kawasaki disease (KD), the leading cause of acquired cardiac disease among children, is often associated with myocarditis that may lead to long-term myocardial dysfunction and fibrosis. Although those myocardial changes develop during the acute phase, they may persist for decades and closely correlate with long-term myocardial sequelae. Using the Lactobacillus casei cell wall extract-induced (LCWE-induced) KD vasculitis murine model, we investigated long-term cardiovascular sequelae, such as myocardial dysfunction, fibrosis, and coronary microvascular lesions following adrenergic stimuli after established KD vasculitis. We found that adrenergic stimulation with isoproterenol following LCWE-induced KD vasculitis in mice was associated with increased risk of cardiac hypertrophy and myocardial fibrosis, diminished ejection fraction, and increased serum levels of brain natriuretic peptide. Myocardial fibrosis resulting from pharmacologic-induced exercise after KD development was IL-1 signaling dependent and was associated with a significant reduction in myocardial capillary CD31 expression, indicative of a rarefied myocardial capillary bed. These observations suggest that adrenergic stimulation after KD vasculitis may lead to cardiac hypertrophy and bridging fibrosis in the myocardium in the LCWE-induced KD vasculitis mouse model and that this process involves IL-1 signaling and diminished microvascular circulation in the myocardium.</abstract><cop>United States</cop><pub>American Society for Clinical Investigation</pub><pmid>30728329</pmid><doi>10.1172/jci.insight.126279</doi><orcidid>https://orcid.org/0000-0002-1432-006X</orcidid><orcidid>https://orcid.org/0000-0001-5570-8928</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 2379-3708
ispartof JCI insight, 2019-02, Vol.4 (3)
issn 2379-3708
2379-3708
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6413776
source EZB-FREE-00999 freely available EZB journals; PubMed Central
title Myocardial fibrosis after adrenergic stimulation as a long-term sequela in a mouse model of Kawasaki disease vasculitis
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T00%3A42%3A25IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Myocardial%20fibrosis%20after%20adrenergic%20stimulation%20as%20a%20long-term%20sequela%20in%20a%20mouse%20model%20of%20Kawasaki%20disease%20vasculitis&rft.jtitle=JCI%20insight&rft.au=Matundan,%20Harry%20H&rft.date=2019-02-07&rft.volume=4&rft.issue=3&rft.issn=2379-3708&rft.eissn=2379-3708&rft_id=info:doi/10.1172/jci.insight.126279&rft_dat=%3Cproquest_pubme%3E2204684107%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2204684107&rft_id=info:pmid/30728329&rfr_iscdi=true