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Dysregulated Expression of the Nuclear Exosome Targeting Complex Component Rbm7 in Nonhematopoietic Cells Licenses the Development of Fibrosis.

Abstract：

:Fibrosis is an incurable disorder of unknown etiology. Segregated-nucleus-containing atypical monocytes (SatMs) are critical for the development of fibrosis. Here we examined the mechanisms that recruit SatMs to pre-fibrotic areas. A screen based on cytokine expression in the fibrotic lung revealed that the chemokine Cxcl12, which is produced by apoptotic nonhematopoietic cells, was essential for SatM recruitment. Analyses of lung tissues at fibrosis onset showed increased expression of Rbm7, a component of the nuclear exosome targeting complex. Rbm7 deletion suppressed bleomycin-induced fibrosis and at a cellular level, suppressed apoptosis of nonhematopoietic cells. Mechanistically, Rbm7 bound to noncoding (nc)RNAs that form subnuclear bodies, including Neat1 speckles. Dysregulated expression of Rbm7 resulted in the nuclear degradation of Neat1 speckles, the dispersion of the DNA repair protein BRCA1, and the triggering of apoptosis. Thus, Rbm7 in epithelial cells plays a critical role in the development of fibrosis by regulating ncRNA decay and thereby the production of chemokines that recruit SatMs.

journal_name

Immunity

journal_title

Immunity

authors

Fukushima K,Satoh T,Sugihara F,Sato Y,Okamoto T,Mitsui Y,Yoshio S,Li S,Nojima S,Motooka D,Nakamura S,Kida H,Standley DM,Morii E,Kanto T,Yanagita M,Matsuura Y,Nagasawa T,Kumanogoh A,Akira S

doi

10.1016/j.immuni.2020.02.007

subject

Has Abstract

pub_date

2020-03-17 00:00:00

pages

542-556.e13

issue

3

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(20)30078-9

journal_volume

52

pub_type

杂志文章

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