NDLI: Thyroid-stimulating hormone induces the secretion of tumor necrosis factor- from 3T3-L1 adipocytes via a protein kinase A-dependent pathway.

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Thyroid-stimulating hormone induces the secretion of tumor necrosis factor- from 3T3-L1 adipocytes via a protein kinase A-dependent pathway.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhang, Y-J Zhao, W. Zhu, M-Y Tang, S-S Zhang, H.
Description	Country affiliation: China Author Affiliation: Zhang YJ ( 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, The Key Laboratory of Hormones and Development (Ministry of Health), Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.)
Abstract	OBJECTIVES: Numerous reports have suggested that thyroid-stimulating hormone (TSH) contributes to insulin resistance in adipocytes by directly stimulating the production of adipokines, such as tumor necrosis factor (TNF- ). The objective of this study was to clarify how TSH regulates TNF- secretion in 3T3-L1 adipocytes and to determine which cell signaling pathways were involved. METHODS: Mouse 3T3-L1 preadipocytes were differentiated into adipocytes and then exposed to 0.1 mIU/ml bovine TSH. The optimal treatment duration was determined by measuring the TNF- concentration in the medium by ELISA. Thereafter, adipocytes were treated with 0.01, 0.1, and 1.0 mIU/ml bovine TSH, and the optimal TSH dose was determined. To decrease TSHR expression, TSHR shRNA was transfected into adipocytes, and the silencing was confirmed by Western blotting. The TSH signaling pathways responsible for regulating TNF- secretion were studied. Phospho-NF-κBp65 Ser276 was quantified by Western blotting, and co-immunopreci-pitations were performed to detect the formation of the IκB /PKAc complex. RESULTS: TNF- secretion from adipocytes peaked 4 h after TSH treatment. TSH induced TNF- secretion in a dose-dependent manner, which was almost completely inhibited by TSHR shRNA. There was a significant positive correlation between phospho-NF-κBp65 Ser276 levels and TNF- secretion. H89, a cAMP-dependent protein kinase A inhibitor, significantly inhibited the effects of TSH. Bovine TSH and forskolin, which increases intracellular cAMP, simultaneously stimulated TNF- secretion. The IκB /PKAc complex could be detected in TSH-treated cells, but complex formation was inhibited by H89. CONCLUSIONS: TSH stimulated the cAMP-PKA pathway in 3T3-L1 adipocytes to increase TNF- secretion.
File Format	HTM / HTML
ISSN	09477349
Issue Number	8
Volume Number	121
e-ISSN	14393646
Journal	Experimental and Clinical Endocrinology & Diabetes
Language	English
Publisher	Thieme
Publisher Date	2013-08-01
Publisher Place	Germany
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Endocrinology Adipocytes Drug Effects Cyclic Amp-dependent Protein Kinases Physiology Thyrotropin Pharmacology Tumor Necrosis Factor-alpha Secretion 3t3-l1 Cells Animals Mice Nf-kappa B Metabolism Rna, Small Interfering Receptors, Thyrotropin Genetics Signal Transduction Journal Article
Alternative Title	Thyroid-stimulating hormone induces the secretion of tumor necrosis factor- from 3T3-L1 adipocytes via a protein kinase A-dependent pathway
Content Type	Text
Resource Type	Article
Subject	Endocrinology, Diabetes and Metabolism Internal Medicine Endocrinology

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