ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
β-Arrestin-1 mediates thyrotropin-enhanced osteoblast differentiation.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 60 citations in OpenAlex.
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- How does Hashimoto's thyroiditis affect bone metabolism?Reviews in endocrine & metabolic disorders · 2023Review
- Possible molecular exploration of herbal pair Haizao-Kunbu in the treatment of Graves' disease by network pharmacology, molecular docking, and molecular dynamic analysis.Frontiers in endocrinology · 2023Article
- A review of TSHR- and IGF-1R-related pathogenesis and treatment of Graves' orbitopathy.Frontiers in immunology · 2023Review
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- Rhythm disturbance in osteoarthritis.Cell communication and signaling : CCS · 2022Review
- Thyroid-Stimulating Hormone Favors Runx2-Mediated Matrix Mineralization in HOS and SaOS2 Cells: An In Vitro and In Silico Approach.Molecules (Basel, Switzerland) · 2022Article
- Thyrotropin, Hyperthyroidism, and Bone Mass.The Journal of clinical endocrinology and metabolism · 2021Review
- Expression and Role of Thyrotropin Receptors in Proopiomelanocortin-Producing Pituitary Cells.Thyroid : official journal of the American Thyroid Association · 2021Article
- Transcriptomics-based analysis of the mechanism by which Wang-Bi capsule alleviates joint destruction in rats with collagen-induced arthritis.Chinese medicine · 2021Article
- Thyroid-stimulating hormone decreases the risk of osteoporosis by regulating osteoblast proliferation and differentiation.BMC endocrine disorders · 2021Article
- Orbital Signaling in Graves' Orbitopathy.Frontiers in endocrinology · 2021Review
- Modulating TSH Receptor Signaling for Therapeutic Benefit.European thyroid journal · 2020Article
- Is There Evidence for IGF1R-Stimulating Abs in Graves' Orbitopathy Pathogenesis?International journal of molecular sciences · 2020Review
- TSH Elicits Cell-Autonomous, Biphasic Responses: A Mechanism Inhibiting Hyperstimulation.Endocrinology · 2020Article
- Graves' disease.Nature reviews. Disease primers · 2020Review
- TSH/IGF1 receptor crosstalk: Mechanism and clinical implications.Pharmacology & therapeutics · 2020Review
- β-Arrestin 1 in Thyrotropin Receptor Signaling in Bone: Studies in Osteoblast-Like Cells.Frontiers in endocrinology · 2020Review
- Thyrotropin Causes Dose-dependent Biphasic Regulation of cAMP Production Mediated by GMolecular pharmacology · 2020Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Thyrotropin (TSH) activation of the TSH receptor (TSHR), a 7-transmembrane-spanning receptor (7TMR), may have osteoprotective properties by direct effects on bone. TSHR activation by TSH phosphorylates protein kinases AKT1, p38α, and ERK1/2 in some cells. We found TSH-induced phosphorylation of these kinases in 2 cell lines engineered to express TSHRs, human embryonic kidney HEK-TSHR cells and human osteoblastic U2OS-TSHR cells. In U2OS-TSHR cells, TSH up-regulated pAKT1 (7.1±0.5-fold), p38α (2.9±0.4-fold), and pERK1/2 (3.1±0.2-fold), whereas small molecule TSHR agonist C2 had no or little effect on pAKT1 (1.8±0.08-fold), p38α (1.2±0.09-fold), and pERK1/2 (1.6±0.19-fold). Furthermore, TSH increased expression of osteoblast marker genes ALPL (8.2±4.6-fold), RANKL (21±5.9-fold), and osteopontin (OPN; 17±5.3-fold), whereas C2 had little effect (ALPL, 1.7±0.5-fold; RANKL, 1.3±0.6-fold; and OPN, 2.2±0.7-fold). β-Arrestin-1 and -2 can mediate activatory signals by 7TMRs. TSH stimulated translocation of β-arrestin-1 and -2 to TSHR, whereas C2 failed to translocate either β-arrestin. Down-regulation of β-arrestin-1 by siRNA inhibited TSH-stimulated phosphorylation of ERK1/2, p38α, and AKT1, whereas down-regulation of β-arrestin-2 increased phosphorylation of AKT1 in both cell types and of ERK1/2 in HEK-TSHR cells. Knockdown of β-arrestin-1 inhibited TSH-stimulated up-regulation of mRNAs for OPN by 87 ± 1.7% and RANKL by 73 ± 2.4%, and OPN secretion by 74 ± 10%. We conclude that TSH enhances osteoblast differentiation in U2OS cells that is, in part, caused by activatory signals mediated by β-arrestin-1.
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