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Activation of the beta 2-adrenergic receptor promotes growth and differentiation in thyroid cells.
Author(s) -
René Hen,
Richard Axel,
Silvana Obici
Publication year - 1989
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.86.12.4785
Subject(s) - endocrinology , receptor , medicine , thyroid , agonist , thyroid hormone receptor , thyroid hormone receptor beta , cyclase , adrenergic receptor , adenylate kinase , chemistry , biology , microbiology and biotechnology , hormone receptor , cancer , breast cancer
We have introduced the beta 2-adrenergic receptor into the unnatural environment of a thyroid cell to demonstrate that the activation of this receptor initiates diverse cellular programs in different cell types. The thyroid-stimulating hormone (TSH) receptor and the beta 2-adrenergic receptor stimulate a common signaling pathway in distinct populations of cells. In this study, we demonstrate that the activation of the beta 2-adrenergic receptor, transfected into a thyroid epithelial cell, elicits a program of growth and differentiation normally observed with TSH. In thyroid cells expressing beta 2 receptors, the beta 2 agonist isoproterenol activates adenylate cyclase, induces the expression of a thyroid-specific iodide carrier system, and can substitute for TSH to promote growth. Thus, in thyroid cells expressing beta 2-adrenergic receptors, isoproterenol elicits the entire array of thyroid-specific functions normally activated by TSH.

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