The cJUN NH2-terminal kinase (JNK) pathway contributes to mouse mammary gland remodeling during involution

Involution returns the lactating mammary gland to a quiescent state after weaning. The mechanism of involution involves collapse of the mammary epithelial cell compartment. To test whether the cJUN NH 2 -terminal kinase (JNK) signal transduction pathway contributes to involution, we established mice...

Full description

Saved in:
Bibliographic Details
Published in:Cell death and differentiation 2018-09, Vol.25 (9), p.1702-1715
Main Authors: Girnius, Nomeda, Edwards, Yvonne J. K., Davis, Roger J.
Format: Article
Language:English
Subjects:
13/1
13/2
13/51
14/34
14/63
38/90
38/91
631/208/199
631/45/275
64/60
82/29
96/95
Apoptosis
Biochemistry
Biomedical and Life Sciences
Cathepsins
Cattle
Cell Biology
Cell Cycle Analysis
Epithelial cells
Epithelium
Lactation
Life Sciences
Mammary gland
Signal transduction
Smad2 protein
Stat3 protein
Stem Cells
Weaning
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Involution returns the lactating mammary gland to a quiescent state after weaning. The mechanism of involution involves collapse of the mammary epithelial cell compartment. To test whether the cJUN NH 2 -terminal kinase (JNK) signal transduction pathway contributes to involution, we established mice with JNK deficiency in the mammary epithelium. We found that JNK is required for efficient involution. JNK deficiency did not alter the STAT3/5 or SMAD2/3 signaling pathways that have been previously implicated in this process. Nevertheless, JNK promotes the expression of genes that drive involution, including matrix metalloproteases, cathepsins, and BH3-only proteins. These data demonstrate that JNK has a key role in mammary gland involution post lactation.
ISSN:1350-9047
1476-5403
DOI:10.1038/s41418-018-0081-z