ArticleInternational journal of medical sciences2008
IGF-1 regulates cAMP levels in astrocytes through a beta2-adrenergic receptor-dependant mechanism.
Article in International journal of medical sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Insulin-like growth factor-1 (IGF-1) levels in multiple sclerosis patients: A systematic review and meta-analysis.PloS one · 2024Pooled it
- Fluconazole Is Neuroprotective via Interactions with the IGF-1 Receptor.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Genetic and Molecular Biology of Multiple Sclerosis Among Iranian Patients: An Overview.Cellular and molecular neurobiology · 2020Review
- Age-dependent alterations to paraventricular nucleus insulin-like growth factor 1 receptor as a possible link between sympathoexcitation and inflammation.Journal of neurochemistry · 2016Article
- Pharmacological approaches to intervention in hypomyelinating and demyelinating white matter pathology.Neuropharmacology · 2016Review
- A-kinase anchoring proteins: cAMP compartmentalization in neurodegenerative and obstructive pulmonary diseases.British journal of pharmacology · 2014Review
- Klotho regulates retinal pigment epithelial functions and protects against oxidative stress.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Metabolic syndrome as a risk factor for neurological disorders.Cellular and molecular life sciences : CMLS · 2012Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have recently demonstrated that neonatal astrocytes derived from mice lacking beta-2 adrenergic receptors (beta(2)AR) possess higher proliferation rates, as compared to wild-type cells, an attribute that was shown to involve insulin-like growth factor (IGF) signaling. In the present study, we demonstrate that basal cAMP levels in beta(2)AR knockout astrocytes were significantly lower than in wild type cells. Furthermore, treatment with IGF-1 reduced intracellular cAMP levels in wild type astrocytes, yet had no effects on cAMP levels in beta(2)AR deficient astrocytes. Our data suggests that IGF-1 treatment influences cAMP production through a beta(2)AR-dependant mechanism in astrocytes. A deficit of beta(2)AR on astrocytes, as previously reported in multiple sclerosis, may influence cell proliferation, an action which could have implications in processes involved in astrogliosis.
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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.