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 NH2-terminal kinase (JNK) signal transduction pathway contributes to involution, we established mice w...

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Published inCell death and differentiation Vol. 25; no. 9; pp. 1702 - 1715
Main Authors Girnius, Nomeda, Edwards, Yvonne J. K., Davis, Roger J.
Format Journal Article
LanguageEnglish
Published Rome Nature Publishing Group 01.09.2018
Nature Publishing Group UK
Subjects
Cathepsins
Cattle
Epithelial cells
Epithelium
Lactation
Mammary gland
Signal transduction
Smad2 protein
Stat3 protein
Weaning
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Abstract 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 NH2-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.
AbstractList 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 NH2-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.
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.
Author Edwards, Yvonne J K
Girnius, Nomeda
Davis, Roger J
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Snippet Involution returns the lactating mammary gland to a quiescent state after weaning. The mechanism of involution involves collapse of the mammary epithelial cell...
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StartPage 1702
SubjectTerms Cathepsins
Cattle
Epithelial cells
Epithelium
Lactation
Mammary gland
Signal transduction
Smad2 protein
Stat3 protein
Weaning
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Title The cJUN NH2-terminal kinase (JNK) pathway contributes to mouse mammary gland remodeling during involution
URI https://www.proquest.com/docview/2108829633/abstract/
https://search.proquest.com/docview/2011615930
https://pubmed.ncbi.nlm.nih.gov/PMC6143629
Volume 25
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