Retinoids and glucocorticoids have opposite effects on actin cytoskeleton rearrangement in hippocampal HT22 cells.
The International Journal of Biochemistry & Cell Biology. 2016-02-01; 71: 102-110
DOI: 10.1016/j.biocel.2015.12.014
Lire sur PubMed
1. Int J Biochem Cell Biol. 2016 Feb;71:102-10. doi: 10.1016/j.biocel.2015.12.014.
Epub 2015 Dec 31.
Retinoids and glucocorticoids have opposite effects on actin cytoskeleton
rearrangement in hippocampal HT22 cells.
Hélène R(1), Julie B(2), Aloïs L(1), Marie-Pierre M(1), Véronique P(3), Anabelle
R(1), Jean-Benoît C(4).
Author information:
(1)INRA, Nutrition et neurobiologie intégrée, UMR 1286, 33076 Bordeaux, France;
University Bordeaux, Nutrition et neurobiologie intégrée, UMR 1286, 33076
Bordeaux, France.
(2)University Bordeaux, Nutrition et neurobiologie intégrée, UMR 1286, 33076
Bordeaux, France; Laboratoire d’Hormonologie, Service de médecine nucléaire, CHU
Bordeaux, 33604 Pessac, France.
(3)University Bordeaux, Nutrition et neurobiologie intégrée, UMR 1286, 33076
Bordeaux, France; IPB, Nutrition et neurobiologie intégrée, UMR 1286, 33076
Bordeaux, France.
(4)University Bordeaux, Nutrition et neurobiologie intégrée, UMR 1286, 33076
Bordeaux, France; Laboratoire d’Hormonologie, Service de médecine nucléaire, CHU
Bordeaux, 33604 Pessac, France. Electronic address:
.
A chronic excess of glucocorticoids elicits deleterious effects in the
hippocampus. Conversely, retinoic acid plays a major role in aging brain
plasticity. As synaptic plasticity depends on mechanisms related to cell
morphology, we investigated the involvement of retinoic acid and glucocorticoids
in the remodelling of the HT22 neurons actin cytoskeleton. Cells exhibited a
significantly more elongated shape with retinoic acid and a rounder shape with
dexamethasone; retinoic acid reversed the effects of dexamethasone. Actin
expression and abundance were unchanged by retinoic acid or dexamethasone but
F-actin organization was dramatically modified. Indeed, retinoic acid and
dexamethasone increased (70 ± 7% and 176 ± 5%) cortical actin while retinoic acid
suppressed the effect of dexamethasone (90 ± 6%). Retinoic acid decreased (-22 ±
9%) and dexamethasone increased (134 ± 16%) actin stress fibres. Retinoic acid
also suppressed the effect of dexamethasone (-21 ± 7%). Spectrin is a key protein
in the actin network remodelling. Its abundance was decreased by retinoic acid
and increased by dexamethasone (-21 ± 11% and 52 ± 10%). However, retinoic acid
did not modify the effect of dexamethasone (48 ± 7%). Calpain activity on
spectrin was increased by retinoic acid and decreased by dexamethasone (26 ± 14%
and -57 ± 5%); retinoic acid mildly but significantly modified the effect of
dexamethasone (-44 ± 7%). The calpain inhibitor calpeptin suppressed the effects
of retinoic acid and dexamethasone on cell shape and actin stress fibres
remodelling but did not modify the effects on cortical actin. Retinoic acid and
dexamethasone have a dramatic but mainly opposite effect on actin cytoskeleton
remodelling. These effects originate, at least partly, from calpain activity.
Copyright © 2016 Elsevier Ltd. All rights reserved.
DOI: 10.1016/j.biocel.2015.12.014
PMID: 26748244 [Indexed for MEDLINE]