Downregulation of stanniocalcin 1 is responsible for sorafenib-induced cardiotoxicity

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Downregulation of stanniocalcin 1 is responsible for sorafenib-induced cardiotoxicity

Persistent ID (NDL): info:ndljp/pid/11976972

Material type: 博士論文

Author: Kawabata, Miko

Publisher: 三重大学

Publication date: 2014-12-10

Material Format: Digital

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Name of awarding university/degree: 三重大学,博士(医学)

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Note (General)：: application/pdfSorafenib is associated with adverse cardiac effects, including left ventricular dysfunction. However, the precise mechanism remains un...

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Material Type: 博士論文
Title: Downregulation of stanniocalcin 1 is responsible for sorafenib-induced cardiotoxicity
Author/Editor: Kawabata, Miko
Author Heading: Kawabata, Miko
Publication, Distribution, etc.: 三重大学
Publication Date: 2014-12-10
Publication Date (W3CDTF): 2014-12-10
Degree grantor/type: 三重大学
Date Granted: 2014-12-10
Date Granted (W3CDTF): 2014-12-10
Dissertation Number: 甲医学第1692号
Degree Type: 博士(医学)
Conferring No. (Dissertation): 甲医学第1692号
Text Language Code: eng
Alias of Author: カワバタ, ミコ
川端, 美湖
Subject Heading: sorafenib
stanniocalcin 1
cardiotoxicity
zebrafish
reactive oxygen species
Target Audience: 一般
Note (General): application/pdf
Sorafenib is associated with adverse cardiac effects, including left ventricular dysfunction. However, the precise mechanism remains unclear. Here, we aimed to establish the genes responsible for this cardiotoxicity using zebrafish and human cardiomyocytes. Fluorescent cardiac imaging using pigmentless zebrafish with green fluorescent protein hearts revealed that the ventricular dimensions of the longitudinal axis with sorafenib were significantly shorter than those of the control group. Transcriptome analysis of their hearts revealed that stanniocalcin 1 (stc1) was downregulated by sorafenib. stc1 knockdown in zebrafish revealed that reduction of stc1 decreased the longitudinal dimensions of zebrafish ventricles, similar to that which occurs during sorafenib treatment. STC1 downregulation and cytotoxicity were also seen in human cardiomyocytes exposed to sorafenib. To clarify the molecular function of stc1 in sorafenib-induced cardiotoxicity, we focused on oxidative stress in cardiomyocytes treated with sorafenib. Reactive oxygen species (ROS) production significantly increased in both species of human cardiomyocytes and zebrafish exposed to sorafenib and STC1 knockdown compared with the controls. Finally, we found that forced expression of stc1 normalized impairment, decreasing the longitudinal dimensions in zebrafish treated with sorafenib. Our study demonstrated that STC1 plays a protective role against ventricular dysfunction and ROS overproduction, which are induced by sorafenib treatment. We discovered for the first time that STC1 downregulation is responsible for sorafenib-induced cardiotoxicity through activated ROS generation.
本文/Department of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan
37p
DOI: info:doi/10.1093/toxsci/kfu235
https://doi.org/info:doi/10.1093/toxsci/kfu235
Persistent ID (NDL): info:ndljp/pid/11976972
https://dl.ndl.go.jp/pid/11976972
Collection: 障害者向け資料
Collection (Materials For Handicapped People:1): テキストデータ
Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
https://dl.ndl.go.jp/collections/A00014
Acquisition Basis: 博士論文（自動収集）
Date Accepted (W3CDTF): 2022-01-10T16:22:37+09:00
Date Created (W3CDTF): 2021-12-13
Format (IMT): application/pdf
Access Restrictions: 国立国会図書館内限定公開
Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
Availability of remote photoduplication service: 可
Periodical Title (URI): http://hdl.handle.net/10076/00020049
https://mie-u.repo.nii.ac.jp/records/14431
Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション
https://dl.ndl.go.jp