TY - JOUR
T1 - Drebrin is induced during myofibroblast differentiation and enhances the production of fibrosis-related genes
AU - Hironaka, Takanori
AU - Ueno, Tomoyuki
AU - Mae, Kyosuke
AU - Yoshimura, Chikashi
AU - Morinaga, Takumi
AU - Horii, Yuma
AU - Nagasaka, Akiomi
AU - Kurose, Hitoshi
AU - Nakaya, Michio
N1 - Funding Information:
We are grateful to Mr. K. Fukuyama for contribution to the early stages of this work. This study was supported by grants from Grants-in-Aid for Scientific Research (KAKENHI) [to M.N. (17H03984, 17H05510, 20H03383), A.N. (19K07122) and H.K. (17H01525)]; The Takeda Science Foundation, The Mochida Memorial Foundation for Medical and Pharmaceutical Research, MSD Life Science Foundation, Senri Life Science Foundation, GSK Japan Research Grant 2016, 2018 Bristol-Myers Squibb KK Research Grants, The Salt Science Research Foundation (to M.N.); from Japan Agency for Medical Research and Development (AMED) (JP19fk0210029 and JP20gm5810030 to M.N.); from Platform Project for Supporting Drug Discovery and Life Science Research (Basis for Supporting Innovative Drug Discovery and Life Science Research (BINDS)) from AMED under Grant Number JP19am0101091; from Grant-in-Aid for JSPS Research Fellow (20J20083 to Y. H.). We appreciate for the technical supports from the Research Support Center, Graduate School of Medical Sciences, Kyushu University.
Funding Information:
We are grateful to Mr. K. Fukuyama for contribution to the early stages of this work. This study was supported by grants from Grants-in-Aid for Scientific Research ( KAKENHI ) [to M.N. ( 17H03984 , 17H05510 , 20H03383 ), A.N. ( 19K07122 ) and H.K. ( 17H01525 )]; The Takeda Science Foundation , The Mochida Memorial Foundation for Medical and Pharmaceutical Research , MSD Life Science Foundation , Senri Life Science Foundation , GSK Japan Research Grant 2016, 2018 Bristol-Myers Squibb KK Research Grants, The Salt Science Research Foundation (to M.N.); from Japan Agency for Medical Research and Development (AMED) ( JP19fk0210029 and JP20gm5810030 to M.N.); from Platform Project for Supporting Drug Discovery and Life Science Research (Basis for Supporting Innovative Drug Discovery and Life Science Research (BINDS)) from AMED under Grant Number JP19am0101091 ; from Grant-in-Aid for JSPS Research Fellow ( 20J20083 to Y. H.). We appreciate for the technical supports from the Research Support Center, Graduate School of Medical Sciences, Kyushu University.
Publisher Copyright:
© 2020 The Authors
PY - 2020/8/20
Y1 - 2020/8/20
N2 - Fibrosis is attributed to excess deposition of extracellular matrix (ECM) proteins including collagen and is associated with various organ dysfunction. This excessive ECM is produced by myofibroblasts, which are differentiated from various cells by a variety of stimuli, represented by TGF-β. However, molecular mechanisms for the regulation of ECM production in myofibroblasts remain obscure. In this study, we demonstrate that the expression of drebrin, which binds to and increases the stability of actin filament in neurons, is increased in mouse hearts and lungs upon fibrosis. Drebrin is mainly expressed in myofibroblasts in the fibrotic hearts and lungs and promotes the expression of fibrosis-related genes, such as Acta2 and Col1a1. Taken together, our study identifies drebrin as a molecule that promotes the production of fibrosis-related genes in myofibroblasts.
AB - Fibrosis is attributed to excess deposition of extracellular matrix (ECM) proteins including collagen and is associated with various organ dysfunction. This excessive ECM is produced by myofibroblasts, which are differentiated from various cells by a variety of stimuli, represented by TGF-β. However, molecular mechanisms for the regulation of ECM production in myofibroblasts remain obscure. In this study, we demonstrate that the expression of drebrin, which binds to and increases the stability of actin filament in neurons, is increased in mouse hearts and lungs upon fibrosis. Drebrin is mainly expressed in myofibroblasts in the fibrotic hearts and lungs and promotes the expression of fibrosis-related genes, such as Acta2 and Col1a1. Taken together, our study identifies drebrin as a molecule that promotes the production of fibrosis-related genes in myofibroblasts.
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U2 - 10.1016/j.bbrc.2020.05.110
DO - 10.1016/j.bbrc.2020.05.110
M3 - Article
C2 - 32703415
AN - SCOPUS:85086765931
VL - 529
SP - 224
EP - 230
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 2
ER -