Loss of autophagy in chondrocytes causes severe growth retardation

Persistent ID (NDL): info:ndljp/pid/11526126

Material type: 博士論文

Author: Horigome, Yoji

Publisher: -

Publication date: 2019-09-20

Material Format: Digital

Capacity, size, etc.: -

Name of awarding university/degree: 新潟大学,博士(医学)

View All

Notes on use at the National Diet Library

本資料は、掲載誌(URI)等のリンク先にある学位授与機関のWebサイトやCiNii Dissertationsから、本文を自由に閲覧できる場合があります。

Notes on use

Note (General)：: Chondrogenesis is accompanied by not only cellular renovation, but also metabolic stress. Therefore, macroautophagy/autophagy is postulated to be invo...

Search by Bookstore

Read this material in an accessible format.

View materials in accessible formats for people with print disabilities (1Type)

Search by Bookstore

Read in Disability Resources

Other Services
- テキストデータ check it on 国立国会図書館デジタルコレクション

Bibliographic Record

You can check the details of this material, its authority (keywords that refer to materials on the same subject, author's name, etc.), etc.

Digital

Material Type: 博士論文
Title: Loss of autophagy in chondrocytes causes severe growth retardation
Author/Editor: Horigome, Yoji
Publication Date: 2019-09-20
Publication Date (W3CDTF): 2019-09-20
Alternative Title: 軟骨細胞におけるオートファジー欠損は重度の成長障害を引き起こす
Degree grantor/type: 新潟大学
Date Granted: 2019-09-20
Date Granted (W3CDTF): 2019-09-20
Dissertation Number: 甲第4632号
Degree Type: 博士(医学)
Conferring No. (Dissertation): 甲第4632号
Text Language Code: eng
Subject Heading: Atg7
autophagy
cartilage
chondrogenesis
glycogenolysis
Note (General): Chondrogenesis is accompanied by not only cellular renovation, but also metabolic stress. Therefore, macroautophagy/autophagy is postulated to be involved in this process. Previous reports have shown that suppression of autophagy during chondrogenesis causes mild growth retardation. However, the role of autophagy in chondrocyte differentiation still largely remains unclear. Here, we show the important role of autophagy on chondrogenesis. The transition of mesenchymal cells to chondrocytes was severely impaired by ablation of Atg7, a gene essential for autophagy. Mice lacking Atg7 after the transition exhibited phenotypes severer than mutant mice in which Atg7 was removed before the transition. Atg7-deficient chondrocytes accumulated large numbers of glycogen granules, hardly proliferate and died specifically in the proliferative zone without any ER-stress signal. Our results suggest that the suppression of autophagy in prechondrogenic cells drives compensatory mechanism(s) that mitigate defective chondrogenesis, and that autophagy participates in glycogenolysis to supply glucose in avascular growth plates.
Autophagy. 2020, 16(3), 501-511.
新大院博(医)甲第892号
元資料の権利情報 : 【○!C】 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.
DOI: info:doi/10.1080/15548627.2019.1628541
https://doi.org/info:doi/10.1080/15548627.2019.1628541
Persistent ID (NDL): info:ndljp/pid/11526126
https://dl.ndl.go.jp/pid/11526126
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): 2020-08-11T22:41:34+09:00
Date Created (W3CDTF): 2020-07-08
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/10191/00051713
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