Open Collections

UBC Faculty Research and Publications

Loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration Pisconti, Addolorata; Banks, Glen B.; Babaeijandaghi, Farshad; Betta, Nicole D.; Rossi, Fabio M. V.; Chamberlain, Jeffrey S.; Olwin, Bradley B.

Abstract

Background: The skeletal muscle stem cell niche provides an environment that maintains quiescent satellite cells, required for skeletal muscle homeostasis and regeneration. Syndecan-3, a transmembrane proteoglycan expressed in satellite cells, supports communication with the niche, providing cell interactions and signals to maintain quiescent satellite cells. Results: Syndecan-3 ablation unexpectedly improves regeneration in repeatedly injured muscle and in dystrophic mice, accompanied by the persistence of sublaminar and interstitial, proliferating myoblasts. Additionally, muscle aging is improved in syndecan-3 null mice. Since syndecan-3 null myofiber-associated satellite cells downregulate Pax7 and migrate away from the niche more readily than wild type cells, syxndecan-3 appears to regulate satellite cell homeostasis and satellite cell homing to the niche. Conclusions: Manipulating syndecan-3 provides a promising target for development of therapies to enhance muscle regeneration in muscular dystrophies and in aged muscle.

Item Metadata

Title
Loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration
Creator
Pisconti, Addolorata; Banks, Glen B.; Babaeijandaghi, Farshad; Betta, Nicole D.; Rossi, Fabio M. V.; Chamberlain, Jeffrey S.; Olwin, Bradley B.
Contributor
University of British Columbia. Biomedical Research Centre
Publisher
BioMed Central
Date Issued
2016-10-04
Description
Background: The skeletal muscle stem cell niche provides an environment that maintains quiescent satellite cells, required for skeletal muscle homeostasis and regeneration. Syndecan-3, a transmembrane proteoglycan expressed in satellite cells, supports communication with the niche, providing cell interactions and signals to maintain quiescent satellite cells. Results: Syndecan-3 ablation unexpectedly improves regeneration in repeatedly injured muscle and in dystrophic mice, accompanied by the persistence of sublaminar and interstitial, proliferating myoblasts. Additionally, muscle aging is improved in syndecan-3 null mice. Since syndecan-3 null myofiber-associated satellite cells downregulate Pax7 and migrate away from the niche more readily than wild type cells, syxndecan-3 appears to regulate satellite cell homeostasis and satellite cell homing to the niche. Conclusions: Manipulating syndecan-3 provides a promising target for development of therapies to enhance muscle regeneration in muscular dystrophies and in aged muscle.
Subject
Satellite cells; Muscle regeneration; Muscular dystrophy; Niche; Cell adhesion; Cell migration; Syndecan-3; Pax7
Genre
Article
Type
Text
Language
eng
Date Available
2018-05-29
Provider
Vancouver : University of British Columbia Library
Rights
Attribution 4.0 International (CC BY 4.0)
DOI
10.14288/1.0367867
URI
http://hdl.handle.net/2429/66168
Affiliation
Other UBC; Non UBC
Citation
Skeletal Muscle. 2016 Oct 04;6(1):34
Publisher DOI
10.1186/s13395-016-0104-8
Peer Review Status
Reviewed
Scholarly Level
Faculty
Copyright Holder
The Author(s).
Rights URI
http://creativecommons.org/licenses/by/4.0/
Aggregated Source Repository
DSpace

Item Media

Item Citations and Data

Rights

Attribution 4.0 International (CC BY 4.0)