ArticleCellular and molecular neurobiology2007
Increased beta(2)-adrenergic receptor activity by thyroid hormone possibly leads to differentiation and maturation of astrocytes in culture.
Article in Cellular and molecular neurobiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Gallic Acid Prevents the Oxidative and Endoplasmic Reticulum Stresses in the Hippocampus of Adult-Onset Hypothyroid Rats.Frontiers in pharmacology · 2021Article
- Docosahexaenoic Acid (DHA) Induced Morphological Differentiation of Astrocytes Is Associated with Transcriptional Upregulation and Endocytosis of βMolecular neurobiology · 2019Article
- Thyroid Hormone-Induced Differentiation of Astrocytes is Associated with Transcriptional Upregulation of β-arrestin-1 and β-adrenergic Receptor-Mediated Endosomal Signaling.Molecular neurobiology · 2016Article
- Role of β-adrenoceptors in glucose uptake in astrocytes using β-adrenoceptor knockout mice.British journal of pharmacology · 2011Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
(1) Our earlier studies indicate a downsteam regulatory role of the beta-adrenergic receptor (beta-AR) system in thyroid hormone induced differentiation and maturation of astrocytes. In the present study we have investigated the contributions of the subtypes of beta-AR in the above phenomenon. (2) Primary astrocyte cultures were grown under thyroid hormone deficient as well as under euthyroid conditions. [(125)I]Pindolol ([(125)I]PIN) binding studies showed a gradual increase in the specific binding to beta(2)-AR when observed at 5, 10, 15, and 20 days under both cultural conditions. Thyroid hormone caused an increase in binding of [(125)I]PIN to beta(2)-AR compared to thyroid hormone deficient controls at all ages of astrocyte culture. (3) Saturation studies using [(125)I]PIN in astrocyte membranes prepared from 20-day-old cultures showed a significant increase in the affinity of the receptors (K (D)) in the thyroid hormone treated cells without any change in receptor number (B (max)). (4) beta(2)-AR mRNA levels were measured by real-time PCR during ontogenic development as well as during exposure of 10-day-old hypothyroid cultures to normal levels of thyroid hormone for 2, 6, 12, and 24 h. None of the conditions caused any significant change in the beta(2)-adrenergic receptor mRNA levels when compared with corresponding hypothyroid controls. (5) Over expression of beta(2)-AR cDNA in hypothyroid astrocytes caused morphological transformation in spite of the absence of thyroid hormone in the medium. (6) Taken together, results suggest thyroid hormone causes a selective increase in [(125)I]PIN binding to beta(2)-AR due to increase in receptor affinity, which may lead to maturation of astrocytes.
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