Rbm7 in Structural Cells: A NEAT Way to Control Fibrosis

Hamida Hammad; Bart N Lambrecht

doi:10.1016/j.immuni.2020.02.008

Rbm7 in Structural Cells: A NEAT Way to Control Fibrosis

Immunity. 2020 Mar 17;52(3):429-431. doi: 10.1016/j.immuni.2020.02.008.

Authors

Hamida Hammad¹, Bart N Lambrecht²

Affiliations

¹ Laboratory of Mucosal Immunology and Immunoregulation, VIB Center for Inflammation Research, Ghent, Belgium; Department of Internal Medicine and Pediatrics, Ghent University, Ghent, Belgium. Electronic address: hamida.hammad@ugent.be.
² Laboratory of Mucosal Immunology and Immunoregulation, VIB Center for Inflammation Research, Ghent, Belgium; Department of Internal Medicine and Pediatrics, Ghent University, Ghent, Belgium; Department of Pulmonary Medicine, Erasmus Medical Center, Rotterdam, the Netherlands.

PMID: 32187513
DOI: 10.1016/j.immuni.2020.02.008

Abstract

The initial molecular events and the cell type(s) responsible for the development of fibrosis are unclear. Fukushima, Satoh, et al. find that increased expression of the nuclear exosome targeting complex component Rbm7 in lung epithelial cells promotes the degradation of the long non-coding RNA NEAT1, impairs DNA repair, and triggers apoptosis. Dying epithelial cells release chemokines that recruit atypical monocytes, which drive tissue fibrosis.

Publication types

Comment

MeSH terms

Cell Nucleus
Exosomes*
Fibrosis
Humans
RNA, Long Noncoding*
RNA-Binding Proteins

Substances

RBM7 protein, human
RNA, Long Noncoding
RNA-Binding Proteins