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Divergent roles for Clusterin in Lung Injury and Repair.

Abstract：

:Lung fibrosis is an unabated wound healing response characterized by the loss and aberrant function of lung epithelial cells. Herein, we report that extracellular Clusterin promoted epithelial cell apoptosis whereas intracellular Clusterin maintained epithelium viability during lung repair. Unlike normal and COPD lungs, IPF lungs were characterized by significantly increased extracellular Clusterin whereas the inverse was evident for intracellular Clusterin. In vitro and in vivo studies demonstrated that extracellular Clusterin promoted epithelial cell apoptosis while intercellular Clusterin modulated the expression of the DNA repair proteins, MSH2, MSH6, OGG1 and BRCA1. The fibrotic response in Clusterin deficient (CLU-/-) mice persisted after bleomycin and it was associated with increased DNA damage, reduced DNA repair responses, and elevated cellular senescence. Remarkably, this pattern mirrored that observed in IPF lung tissues. Together, our results show that cellular localization of Clusterin leads to divergent effects on epithelial cell regeneration and lung repair during fibrosis.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Habiel DM,Camelo A,Espindola M,Burwell T,Hanna R,Miranda E,Carruthers A,Bell M,Coelho AL,Liu H,Pilataxi F,Clarke L,Grant E,Lewis A,Moore B,Knight DA,Hogaboam CM,Murray LA

doi

10.1038/s41598-017-15670-5

subject

Has Abstract

pub_date

2017-11-13 00:00:00

pages

15444

issue

1

issn

2045-2322

pii

10.1038/s41598-017-15670-5

journal_volume

7

pub_type

杂志文章

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