P2590A liver-derived secretory protein, selenoprotein P causes pressure overload-induced cardiac hypertrophys

P2590A liver-derived secretory protein, selenoprotein P causes pressure overload-induced cardiac hypertrophys

Abstract Background Hepatokine selenoprotein P (SeP) contributes to insulin resistance and hyperglycemia in patients with type 2 diabetes. Inhibition of SeP protects the heart from ischemia reperfusion injury and serum levels of SeP are elevated in patients with heart failure with reduced ejection f...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:European heart journal 2019-10, Vol.40 (Supplement_1)
Hauptverfasser: Usui, S, Takashima, S, Inoue, O, Goten, C, Takeda, Y, Yamaguchi, K, Murai, H, Kaneko, S, Takamura, M
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page
container_issue Supplement_1
container_start_page
container_title European heart journal
container_volume 40
creator Usui, S
Takashima, S
Inoue, O
Goten, C
Takeda, Y
Yamaguchi, K
Murai, H
Kaneko, S
Takamura, M
description Abstract Background Hepatokine selenoprotein P (SeP) contributes to insulin resistance and hyperglycemia in patients with type 2 diabetes. Inhibition of SeP protects the heart from ischemia reperfusion injury and serum levels of SeP are elevated in patients with heart failure with reduced ejection fraction. Objective We investigated the role of SeP in the regulation of cardiac remodeling in response to pressure overload. Methods and results To examine the role of SeP in cardiac remodeling, transverse aortic constriction (TAC) was subjected to SeP knockout (KO) and wild-type (WT) mice for 2 weeks. Hepatic expression of SeP in WT was significantly increased by TAC. LV weight/tibial length (TL) was significantly smaller in SeP KO mice than in WT mice (6.75±0.24 vs 8.33±0.32, p
doi_str_mv 10.1093/eurheartj/ehz748.0916
format Article
fullrecord <record><control><sourceid>oup_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1093_eurheartj_ehz748_0916</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1093/eurheartj/ehz748.0916</oup_id><sourcerecordid>10.1093/eurheartj/ehz748.0916</sourcerecordid><originalsourceid>FETCH-LOGICAL-c876-67193196ca44b6cf94a45644fa955dc67e9200c40202d12960166a2dd4e36f823</originalsourceid><addsrcrecordid>eNqNkMtqwzAQRUVpoWnaTyj4A-pkJEtjaxlCXxBoFll0Z1RpjB2cyEh2wf36OiR03dVl5nLu4jD2yGHBQWdLGkJNJvT7JdU_uSwWoDlesRlXQqQapbpmM-BapYjF5y27i3EPAAVynLHDVigNq6RtvimkjsKULolkA_U-jEkXfE_N8Wl6tXT0lzPZJtYMkeLUU4xDoMRPfOuNS5ujG-y0YU1wjbFJPXYU-uC7eoz37KYybaSHS87Z7uV5t35LNx-v7-vVJrVFjinmXGdcozVSfqGttDRSoZSV0Uo5izlpAWAlCBCOC43AEY1wTlKGVSGyOVPnWRt8jIGqsgvNwYSx5FCelJV_ysqzsvKkbOLgzPmh-yfyC7HSdZU</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>P2590A liver-derived secretory protein, selenoprotein P causes pressure overload-induced cardiac hypertrophys</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Oxford University Press Journals All Titles (1996-Current)</source><source>Alma/SFX Local Collection</source><creator>Usui, S ; Takashima, S ; Inoue, O ; Goten, C ; Takeda, Y ; Yamaguchi, K ; Murai, H ; Kaneko, S ; Takamura, M</creator><creatorcontrib>Usui, S ; Takashima, S ; Inoue, O ; Goten, C ; Takeda, Y ; Yamaguchi, K ; Murai, H ; Kaneko, S ; Takamura, M</creatorcontrib><description>Abstract Background Hepatokine selenoprotein P (SeP) contributes to insulin resistance and hyperglycemia in patients with type 2 diabetes. Inhibition of SeP protects the heart from ischemia reperfusion injury and serum levels of SeP are elevated in patients with heart failure with reduced ejection fraction. Objective We investigated the role of SeP in the regulation of cardiac remodeling in response to pressure overload. Methods and results To examine the role of SeP in cardiac remodeling, transverse aortic constriction (TAC) was subjected to SeP knockout (KO) and wild-type (WT) mice for 2 weeks. Hepatic expression of SeP in WT was significantly increased by TAC. LV weight/tibial length (TL) was significantly smaller in SeP KO mice than in WT mice (6.75±0.24 vs 8.33±0.32, p&lt;0.01). Lung weight/TL was significantly smaller in SeP KO than in WT mice (10.46±0.44 vs 16.38±1.12, p&lt;0.05). TAC-induced cardiac upregulation of the fetal type genes, including atrial and brain natriuretic factors, was significantly attenuated in SeP KO compared to WT. Furthermore, azan staining revealed that there was significantly less interstitial fibrosis in hearts after TAC in SeP KO than in WT mice. To determine whether hepatic overexpression of SeP affects TAC-induced cardiac hypertrophy, a hydrodynamic injection method was used to generate mice that overexpress SeP mRNA in the liver. Hepatic overexpression of SeP in SeP KO mice lead to a significant increase in LV weight/TL and Lung weight/TL after TAC compared to that in other SeP KO mice. Conclusions These results suggest that cardiac pressure overload induced hepatic expression of SeP and the absence of endogenous SeP attenuated cardiac hypertrophy, dysfunction and fibrosis in response to pressure overload in mice. SeP possibly plays a maladaptive role against progression of heart failure through the liver-heart axis.</description><identifier>ISSN: 0195-668X</identifier><identifier>EISSN: 1522-9645</identifier><identifier>DOI: 10.1093/eurheartj/ehz748.0916</identifier><language>eng</language><publisher>Oxford University Press</publisher><ispartof>European heart journal, 2019-10, Vol.40 (Supplement_1)</ispartof><rights>Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com. 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,1581,27911,27912</link.rule.ids></links><search><creatorcontrib>Usui, S</creatorcontrib><creatorcontrib>Takashima, S</creatorcontrib><creatorcontrib>Inoue, O</creatorcontrib><creatorcontrib>Goten, C</creatorcontrib><creatorcontrib>Takeda, Y</creatorcontrib><creatorcontrib>Yamaguchi, K</creatorcontrib><creatorcontrib>Murai, H</creatorcontrib><creatorcontrib>Kaneko, S</creatorcontrib><creatorcontrib>Takamura, M</creatorcontrib><title>P2590A liver-derived secretory protein, selenoprotein P causes pressure overload-induced cardiac hypertrophys</title><title>European heart journal</title><description>Abstract Background Hepatokine selenoprotein P (SeP) contributes to insulin resistance and hyperglycemia in patients with type 2 diabetes. Inhibition of SeP protects the heart from ischemia reperfusion injury and serum levels of SeP are elevated in patients with heart failure with reduced ejection fraction. Objective We investigated the role of SeP in the regulation of cardiac remodeling in response to pressure overload. Methods and results To examine the role of SeP in cardiac remodeling, transverse aortic constriction (TAC) was subjected to SeP knockout (KO) and wild-type (WT) mice for 2 weeks. Hepatic expression of SeP in WT was significantly increased by TAC. LV weight/tibial length (TL) was significantly smaller in SeP KO mice than in WT mice (6.75±0.24 vs 8.33±0.32, p&lt;0.01). Lung weight/TL was significantly smaller in SeP KO than in WT mice (10.46±0.44 vs 16.38±1.12, p&lt;0.05). TAC-induced cardiac upregulation of the fetal type genes, including atrial and brain natriuretic factors, was significantly attenuated in SeP KO compared to WT. Furthermore, azan staining revealed that there was significantly less interstitial fibrosis in hearts after TAC in SeP KO than in WT mice. To determine whether hepatic overexpression of SeP affects TAC-induced cardiac hypertrophy, a hydrodynamic injection method was used to generate mice that overexpress SeP mRNA in the liver. Hepatic overexpression of SeP in SeP KO mice lead to a significant increase in LV weight/TL and Lung weight/TL after TAC compared to that in other SeP KO mice. Conclusions These results suggest that cardiac pressure overload induced hepatic expression of SeP and the absence of endogenous SeP attenuated cardiac hypertrophy, dysfunction and fibrosis in response to pressure overload in mice. SeP possibly plays a maladaptive role against progression of heart failure through the liver-heart axis.</description><issn>0195-668X</issn><issn>1522-9645</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNqNkMtqwzAQRUVpoWnaTyj4A-pkJEtjaxlCXxBoFll0Z1RpjB2cyEh2wf36OiR03dVl5nLu4jD2yGHBQWdLGkJNJvT7JdU_uSwWoDlesRlXQqQapbpmM-BapYjF5y27i3EPAAVynLHDVigNq6RtvimkjsKULolkA_U-jEkXfE_N8Wl6tXT0lzPZJtYMkeLUU4xDoMRPfOuNS5ujG-y0YU1wjbFJPXYU-uC7eoz37KYybaSHS87Z7uV5t35LNx-v7-vVJrVFjinmXGdcozVSfqGttDRSoZSV0Uo5izlpAWAlCBCOC43AEY1wTlKGVSGyOVPnWRt8jIGqsgvNwYSx5FCelJV_ysqzsvKkbOLgzPmh-yfyC7HSdZU</recordid><startdate>20191001</startdate><enddate>20191001</enddate><creator>Usui, S</creator><creator>Takashima, S</creator><creator>Inoue, O</creator><creator>Goten, C</creator><creator>Takeda, Y</creator><creator>Yamaguchi, K</creator><creator>Murai, H</creator><creator>Kaneko, S</creator><creator>Takamura, M</creator><general>Oxford University Press</general><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20191001</creationdate><title>P2590A liver-derived secretory protein, selenoprotein P causes pressure overload-induced cardiac hypertrophys</title><author>Usui, S ; Takashima, S ; Inoue, O ; Goten, C ; Takeda, Y ; Yamaguchi, K ; Murai, H ; Kaneko, S ; Takamura, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c876-67193196ca44b6cf94a45644fa955dc67e9200c40202d12960166a2dd4e36f823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Usui, S</creatorcontrib><creatorcontrib>Takashima, S</creatorcontrib><creatorcontrib>Inoue, O</creatorcontrib><creatorcontrib>Goten, C</creatorcontrib><creatorcontrib>Takeda, Y</creatorcontrib><creatorcontrib>Yamaguchi, K</creatorcontrib><creatorcontrib>Murai, H</creatorcontrib><creatorcontrib>Kaneko, S</creatorcontrib><creatorcontrib>Takamura, M</creatorcontrib><collection>CrossRef</collection><jtitle>European heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Usui, S</au><au>Takashima, S</au><au>Inoue, O</au><au>Goten, C</au><au>Takeda, Y</au><au>Yamaguchi, K</au><au>Murai, H</au><au>Kaneko, S</au><au>Takamura, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>P2590A liver-derived secretory protein, selenoprotein P causes pressure overload-induced cardiac hypertrophys</atitle><jtitle>European heart journal</jtitle><date>2019-10-01</date><risdate>2019</risdate><volume>40</volume><issue>Supplement_1</issue><issn>0195-668X</issn><eissn>1522-9645</eissn><abstract>Abstract Background Hepatokine selenoprotein P (SeP) contributes to insulin resistance and hyperglycemia in patients with type 2 diabetes. Inhibition of SeP protects the heart from ischemia reperfusion injury and serum levels of SeP are elevated in patients with heart failure with reduced ejection fraction. Objective We investigated the role of SeP in the regulation of cardiac remodeling in response to pressure overload. Methods and results To examine the role of SeP in cardiac remodeling, transverse aortic constriction (TAC) was subjected to SeP knockout (KO) and wild-type (WT) mice for 2 weeks. Hepatic expression of SeP in WT was significantly increased by TAC. LV weight/tibial length (TL) was significantly smaller in SeP KO mice than in WT mice (6.75±0.24 vs 8.33±0.32, p&lt;0.01). Lung weight/TL was significantly smaller in SeP KO than in WT mice (10.46±0.44 vs 16.38±1.12, p&lt;0.05). TAC-induced cardiac upregulation of the fetal type genes, including atrial and brain natriuretic factors, was significantly attenuated in SeP KO compared to WT. Furthermore, azan staining revealed that there was significantly less interstitial fibrosis in hearts after TAC in SeP KO than in WT mice. To determine whether hepatic overexpression of SeP affects TAC-induced cardiac hypertrophy, a hydrodynamic injection method was used to generate mice that overexpress SeP mRNA in the liver. Hepatic overexpression of SeP in SeP KO mice lead to a significant increase in LV weight/TL and Lung weight/TL after TAC compared to that in other SeP KO mice. Conclusions These results suggest that cardiac pressure overload induced hepatic expression of SeP and the absence of endogenous SeP attenuated cardiac hypertrophy, dysfunction and fibrosis in response to pressure overload in mice. SeP possibly plays a maladaptive role against progression of heart failure through the liver-heart axis.</abstract><pub>Oxford University Press</pub><doi>10.1093/eurheartj/ehz748.0916</doi></addata></record>
fulltext fulltext
identifier ISSN: 0195-668X
ispartof European heart journal, 2019-10, Vol.40 (Supplement_1)
issn 0195-668X
1522-9645
language eng
recordid cdi_crossref_primary_10_1093_eurheartj_ehz748_0916
source Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection
title P2590A liver-derived secretory protein, selenoprotein P causes pressure overload-induced cardiac hypertrophys
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-16T01%3A13%3A06IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-oup_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=P2590A%20liver-derived%20secretory%20protein,%20selenoprotein%20P%20causes%20pressure%20overload-induced%20cardiac%20hypertrophys&rft.jtitle=European%20heart%20journal&rft.au=Usui,%20S&rft.date=2019-10-01&rft.volume=40&rft.issue=Supplement_1&rft.issn=0195-668X&rft.eissn=1522-9645&rft_id=info:doi/10.1093/eurheartj/ehz748.0916&rft_dat=%3Coup_cross%3E10.1093/eurheartj/ehz748.0916%3C/oup_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/&rft_oup_id=10.1093/eurheartj/ehz748.0916&rfr_iscdi=true