ArticleProceedings of the National Academy of Sciences of the United States of America1997
Glucocorticoid receptor pathways are involved in the inhibition of astrocyte proliferation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 145 citations in OpenAlex.
- Immune cells in Alzheimer's disease: insights into pathogenesis and potential therapeutic targets.Medical review (2021) · 2025Review
- Article
- Article
- Review
- Modification of Müller Glial Cell Fate and Proliferation with the Use of Small Molecules.Advances in experimental medicine and biology · 2023Review
- Prenatal glucocorticoid exposure selectively impairs neuroligin 1-dependent neurogenesis by suppressing astrocytic FGF2-neuronal FGFR1 axis.Cellular and molecular life sciences : CMLS · 2022Article
- Review
- Exposure to 2.45 GHz Radiation Triggers Changes in HSP-70, Glucocorticoid Receptors and GFAP Biomarkers in Rat Brain.International journal of molecular sciences · 2021Article
- The combination of acyclovir and dexamethasone protects against Alzheimer's disease-related cognitive impairments in mice.Psychopharmacology · 2020Article
- Cell Adhesion Molecules and Protein Synthesis Regulation in Neurons.Frontiers in molecular neuroscience · 2020Review
- Review
- Domain swapping and SMYD1 interactions with the PWWP domain of human hepatoma-derived growth factor.Scientific reports · 2018Article
- Microglia and Astrocytes in Alzheimer's Disease: Implications for Therapy.Current neuropharmacology · 2018Review
- Common Mechanisms Underlying Epileptogenesis and the Comorbidities of Epilepsy.Cold Spring Harbor perspectives in medicine · 2016Review
- Astroglial Plasticity Is Implicated in Hippocampal Remodelling in Adult Rats Exposed to Antenatal Dexamethasone.Neural plasticity · 2015Article
- A complex mechanism for HDGF-mediated cell growth, migration, invasion, and TMZ chemosensitivity in glioma.Journal of neuro-oncology · 2014Article
- Biomarkers of epileptogenesis: psychiatric comorbidities (?).Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2014Review
- Identifying the cellular targets of drug action in the central nervous system following corticosteroid therapy.ACS chemical neuroscience · 2014Article
- Epilepsy, cognition, and neuropsychiatry (Epilepsy, Brain, and Mind, part 2).Epilepsy & behavior : E&B · 2013Review
- Rapid elevation of calcium concentration in cultured dorsal spinal cord astrocytes by corticosterone.Neurochemical research · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
In earlier studies, the neural cell adhesion molecule, N-CAM, was found to inhibit the proliferation of rat astrocytes both in vitro and in vivo. To identify the gene targets involved, we used subtractive hybridization to examine changes in gene expression that occur after astrocytes are exposed to N-CAM in vitro. While the mRNA levels for N-CAM decreased after such treatment, the levels of mRNAs for glutamine synthetase and calreticulin increased. Since glutamine synthetase and calreticulin are known to be involved in glucocorticoid receptor pathways, we tested a number of steroids for their effects on astrocyte proliferation. Dexamethasone, corticosterone, and aldosterone were all found to inhibit rat cortical astrocyte proliferation in culture in a dose-dependent manner. RU-486, a potent glucocorticoid antagonist, reversed the inhibitory effects of dexamethasone. These observations prompted the hypothesis that the inhibition of proliferation by N-CAM might be mediated through the glucocorticoid receptor pathway. Consistent with this hypothesis, the inhibition of astrocyte proliferation by N-CAM was reversed in part by a number of glucocorticoid antagonists, including RU-486, dehydroepiandrosterone, and progesterone. In transfection experiments with cultured astrocytes, N-CAM treatment increased the expression of a luciferase reporter gene under the control of a minimal promoter linked to a glucocorticoid response element. The enhanced activity of this construct stimulated by N-CAM was abolished in the presence of RU-486. The combined data suggest that astrocyte proliferation is in part regulated by alterations in glucocorticoid receptor pathways.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.