Document Detail


13-Cis-retinoic acid decreases hypothalamic cell number in vitro.
MedLine Citation:
PMID:  20708044     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
13-Cis-retinoic acid (13-cis-RA) causes depression-related behavior in mice. Hypothalamic dysregulation has been implicated in clinical depression. In fact, apoptosis of hypothalamic neurons may lead to depression after myocardial infarction. Our objective was to determine if 13-cis-RA affects cultured hypothalamic cell number. Treatment of GT1-7 hypothalamic cells with 10μM 13-cis-RA for 48h decreased cell growth to 45.6±13% of control. To determine if this decrease in cell number was due to 13-cis-RA acting as an oxidant, cells were treated with 13-cis-RA and ascorbic acid or butylated hydroxyanisole (BHA) for 24 or 48h. Neither antioxidant alleviated the inhibitory affects of 13-cis-RA. In addition, 13-cis-RA treatment did not increase superoxide anion production, indicating 13-cis-RA was not acting as an oxidant. To determine if 13-cis-RA was acting via retinoic acid receptors (RARs) to decrease cell number, GT1-7 cells were treated with 13-cis-RA and the RAR pan-antagonist, AGN 193109. Treatment with the RAR-antagonist blocked the ability of 13-cis-RA to decrease cell number, indicating this phenomenon was a RAR-independent mechanism. We hypothesize that the ability of 13-cis-RA to decrease hypothalamic cell number may contribute to the increased depression-related behaviors observed in mice.
Authors:
Jennifer N Griffin; Daniel Pinali; Kaylan Olds; Na Lu; Lindsay Appleby; Louis Doan; Michelle A Lane
Related Documents :
3181664 - In vivo selection of tumorigenic subline from non-tumorigenic human gastric carcinoma c...
1622394 - A novel mechanism for isoprenaline-stimulated proliferation of rat parotid acinar cells...
1887334 - Gene expression and metastasis of somatic cell hybrids between murine fibroblast cell l...
6308014 - Loss of egf binding and cation transport response during differentiation of mouse neuro...
23703614 - N-glycosylation induces the cthrc1 protein and drives oral cancer cell migration.
9799664 - Expressions and activities of cell cycle regulatory molecules during the transition fro...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-08-11
Journal Detail:
Title:  Neuroscience research     Volume:  68     ISSN:  1872-8111     ISO Abbreviation:  Neurosci. Res.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-10-11     Completed Date:  2011-01-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8500749     Medline TA:  Neurosci Res     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  185-90     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.
Affiliation:
Department of Family and Consumer Sciences, Division of Nutrition and Foods, Texas State University, San Marcos, TX 78666, United States.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Cell Count
Cell Line
Cells, Cultured
Hypothalamus / cytology,  drug effects*,  metabolism
Isotretinoin / pharmacology*
Mice
Neurons / cytology,  drug effects*,  metabolism
Receptors, Retinoic Acid / metabolism
Superoxides / metabolism
Chemical
Reg. No./Substance:
0/Receptors, Retinoic Acid; 11062-77-4/Superoxides; 4759-48-2/Isotretinoin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Protein quality control mechanisms and neurodegenerative disorders: Checks, balances and deadlocks.
Next Document:  (+)-Cholesten-3-one induces differentiation of neural stem cells into dopaminergic neurons through B...