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Meflin/ISLR is a marker of adipose stem and progenitor cells in mice and humans that suppresses white adipose tissue remodeling and fibrosis.

Authors :
Ishihara, Toshikazu
Kato, Katsuhiro
Matsumoto, Kotaro
Tanaka, Miyako
Hara, Akitoshi
Shiraki, Yukihiro
Morisaki, Hidenori
Urano, Yuya
Ando, Ryota
Ito, Kisuke
Mii, Shinji
Esaki, Nobutoshi
Furuhashi, Kazuhiro
Takefuji, Mikito
Suganami, Takayoshi
Murohara, Toyoaki
Enomoto, Atsushi
Source :
Genes to Cells. Oct2024, Vol. 29 Issue 10, p902-920. 19p.
Publication Year :
2024

Abstract

Identifying specific markers of adipose stem and progenitor cells (ASPCs) in vivo is crucial for understanding the biology of white adipose tissues (WAT). PDGFRα‐positive perivascular stromal cells represent the best candidates for ASPCs. This cell lineage differentiates into myofibroblasts that contribute to the impairment of WAT function. However, ASPC marker protein(s) that are functionally crucial for maintaining WAT homeostasis are unknown. We previously identified Meflin as a marker of mesenchymal stem cells (MSCs) in bone marrow and tissue‐resident perivascular fibroblasts in various tissues. We also demonstrated that Meflin maintains the undifferentiated status of MSCs/fibroblasts. Here, we show that Meflin is expressed in WAT ASPCs. A lineage‐tracing experiment showed that Meflin+ ASPCs proliferate in the WAT of obese mice induced by a high‐fat diet (HFD), while some of them differentiate into myofibroblasts or mature adipocytes. Meflin knockout mice fed an HFD exhibited a significant fibrotic response as well as increases in adipocyte cell size and the number of crown‐like structures in WAT, accompanied by impaired glucose tolerance. These data suggested that Meflin expressed by ASPCs may have a role in reducing disease progression associated with WAT dysfunction. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
13569597
Volume :
29
Issue :
10
Database :
Academic Search Index
Journal :
Genes to Cells
Publication Type :
Academic Journal
Accession number :
180110412
Full Text :
https://doi.org/10.1111/gtc.13154