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Periostin deficiency attenuates lipopolysaccharide‐ and obesity‐induced adipose tissue fibrosis
Author(s) -
Yang Yuhan,
Zhang Yanfei,
Zhou Xueliang,
Chen Dandan,
Ouyang Gaoliang,
Liu Yingfu,
Cui Dan
Publication year - 2021
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.14154
Subject(s) - periostin , adipose tissue , matricellular protein , fibrosis , adipose tissue macrophages , medicine , endocrinology , adipocyte , progenitor cell , 3t3 l1 , adipokine , insulin resistance , white adipose tissue , microbiology and biotechnology , biology , stem cell , diabetes mellitus , extracellular matrix
Periostin (POSTN) is a type of matricellular protein, but its functions in adipose fibrosis remain unclear. Here, we found that POSTN expression is significantly increased in mouse adipose tissue after treatment with lipopolysaccharide (LPS) or a high‐fat diet (HFD) and that adipose progenitor cells are the main source of POSTN. In our mouse model of fibrosis, POSTN deletion protected mice from adipose fibrosis, probably through reducing the accumulation of macrophages and promoting adipocyte differentiation of progenitor cells. Taken together, our study demonstrates that POSTN deficiency attenuates adipose tissue fibrosis and improves insulin resistance, providing new insights into the diagnosis and treatment of type II diabetes by targeting adipose tissue fibrosis.