title: Retinoids and glucocorticoids have opposite effects on actin cytoskeleton rearrangement in hippocampal HT22 cells.
abstract: 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.
authors.affiliation: INRA, Nutrition et neurobiologie intégrée, UMR 1286, 33076 Bordeaux, France; University Bordeaux, Nutrition et neurobiologie intégrée, UMR 1286, 33076 Bordeaux, France.
authors.forename: Hélène
authors.initials: H
authors.lastname: Roumes
authors.affiliation: University Bordeaux, Nutrition et neurobiologie intégrée, UMR 1286, 33076 Bordeaux, France; Laboratoire d'Hormonologie, Service de médecine nucléaire, CHU Bordeaux, 33604 Pessac, France.
authors.forename: Julie
authors.initials: J
authors.lastname: Brossaud
authors.affiliation: INRA, Nutrition et neurobiologie intégrée, UMR 1286, 33076 Bordeaux, France; University Bordeaux, Nutrition et neurobiologie intégrée, UMR 1286, 33076 Bordeaux, France.
authors.forename: Aloïs
authors.initials: A
authors.lastname: Lemelletier
authors.affiliation: INRA, Nutrition et neurobiologie intégrée, UMR 1286, 33076 Bordeaux, France; University Bordeaux, Nutrition et neurobiologie intégrée, UMR 1286, 33076 Bordeaux, France.
authors.forename: Marie-Pierre
authors.initials: MP
authors.lastname: Moisan
authors.affiliation: University Bordeaux, Nutrition et neurobiologie intégrée, UMR 1286, 33076 Bordeaux, France; IPB, Nutrition et neurobiologie intégrée, UMR 1286, 33076 Bordeaux, France.
authors.forename: Véronique
authors.initials: V
authors.lastname: Pallet
authors.affiliation: INRA, Nutrition et neurobiologie intégrée, UMR 1286, 33076 Bordeaux, France; University Bordeaux, Nutrition et neurobiologie intégrée, UMR 1286, 33076 Bordeaux, France.
authors.forename: Anabelle
authors.initials: A
authors.lastname: Redonnet
authors.affiliation: 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: jean-benoit.corcuff@u-bordeaux.fr.
authors.forename: Jean-Benoît
authors.initials: JB
authors.lastname: Corcuff
mesh_terms: D008841:Actin Cytoskeleton / Q000187:drug effects* / Q000378:metabolism*; D000199:Actins / Q000378:metabolism; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000235:genetics; D002154:Calpain / Q000378:metabolism; D002460:Cell Line; D003598:Cytoskeletal Proteins / Q000235:genetics; D003907:Dexamethasone / Q000494:pharmacology; D004347:Drug Interactions; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D005938:Glucocorticoids / Q000378:metabolism / Q000494:pharmacology*; D006624:Hippocampus / Q000166:cytology* / Q000187:drug effects*; D006801:Humans; D009419:Nerve Tissue Proteins / Q000235:genetics; D009474:Neurons / Q000166:cytology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012176:Retinoids / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D000199:Actins; D003598:Cytoskeletal Proteins; D005938:Glucocorticoids; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; D012176:Retinoids; C092069:activity regulated cytoskeletal-associated protein; D003907:Dexamethasone; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D002154:Calpain
keywords: Actin cytoskeleton; Glucocorticoid; Hippocampus; Retinoic acid