Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0120672
Title: Estrogens induce rapid cytoskeleton re-organization in human dermal fibroblasts via the non-classical receptor GPR30
Authors: Carnesecchi J.
Malbouyres M.
De Mets R. 
Balland M.
Beauchef G.
Vié K.
Chamot C.
Lionnet C.
Ruggiero F.
Vanacker J.-M.
Keywords: actin
cycloheximide
estradiol
estrogen
estrogen receptor
G protein coupled receptor 30
mitogen activated protein kinase 1
mitogen activated protein kinase 3
phosphatidylinositol 3 kinase
protein tyrosine kinase
short hairpin RNA
vinculin
1,3 benzodioxole derivative
4-(6-bromo-1,3-benzodioxol-5-yl)-3a,4,5,9b-3H-cyclopenta(c)quinoline
estradiol
estrogen
estrogen receptor
estrogen receptor beta
G protein coupled receptor
GPER protein, human
MAPK1 protein, human
mitogen activated protein kinase 1
mitogen activated protein kinase 3
phosphatidylinositol 3 kinase
quinoline derivative
adult
Article
cell migration
cell proliferation
cell shape
cell structure
collagen synthesis
controlled study
cytoskeleton
cytoskeleton reorganization
enzyme activation
female
focal adhesion
human
human cell
inhibition kinetics
primary culture
protein expression
signal transduction
skin fibroblast
agonists
antagonists and inhibitors
dermis
drug effects
fibroblast
metabolism
Adult
Benzodioxoles
Dermis
Estradiol
Estrogen Receptor beta
Estrogens
Female
Fibroblasts
Humans
MAP Kinase Signaling System
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinase 3
Phosphatidylinositol 3-Kinases
Quinolines
Receptors, Estrogen
Receptors, G-Protein-Coupled
Issue Date: 2015
Publisher: Public Library of Science
Citation: Carnesecchi J., Malbouyres M., De Mets R., Balland M., Beauchef G., Vié K., Chamot C., Lionnet C., Ruggiero F., Vanacker J.-M. (2015). Estrogens induce rapid cytoskeleton re-organization in human dermal fibroblasts via the non-classical receptor GPR30. PLoS ONE 10 (3) : e0120672. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0120672
Abstract: The post-menopausal decrease in estrogen circulating levels results in rapid skin deterioration pointing out to a protective effect exerted by these hormones. The identity of the skin cell type responding to estrogens is unclear as are the cellular and molecular processes they elicit. Here, we reported that lack of estrogens induces rapid re-organization of the human dermal fibroblast cytoskeleton resulting in striking cell shape change. This morphological change was accompanied by a spatial re-organization of focal adhesion and a substantial reduction of their number as evidenced by vinculin and actin co-staining. Cell morphology and cytoskeleton organization was fully restored upon 17?-estradiol (E2) addition. Treatment with specific ER antagonists and cycloheximide respectively showed that the E2 acts independently of the classical Estrogen Receptors and that cell shape change is mediated by non-genomic mechanisms. E2 treatment resulted in a rapid and transient activation of ERK1/2 but not Src or PI3K. We show that human fibroblasts express the nonclassical E2 receptor GPR30 and that its agonist G-1 phenocopies the effect of E2. Inhibiting GPR30 through treatment with the G-15 antagonist or specific shRNA impaired E2 effects. Altogether, our data reveal a novel mechanism by which estrogens act on skin fibroblast by regulating cell shape through the non-classical G protein-coupled receptor GPR30 and ERK1/2 activation. © 2015 Carnesecchi et al.
Source Title: PLoS ONE
URI: https://scholarbank.nus.edu.sg/handle/10635/165701
ISSN: 19326203
DOI: 10.1371/journal.pone.0120672
Appears in Collections:Staff Publications
Elements

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
10_1371_journal_pone_0120672.pdf1.7 MBAdobe PDF

OPEN

PublishedView/Download

SCOPUSTM   
Citations

22
checked on Oct 23, 2020

Page view(s)

51
checked on Oct 16, 2020

Download(s)

1
checked on Oct 16, 2020

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.