Regulation of natriuretic peptide receptors by thyrotropin in FRTL-5 rat thyroid cells: evidence for nonguanylate cyclase atrial natriuretic factor-binding sites in cells lacking the natriuretic peptide receptor C.

摘要: Natriuretic peptide receptors (NPR) are expressed in thyroid-derived cells, including the rat FRTL-5 thyroid cell line. We have previously demonstrated that atrial natriuretic factor (ANF) binding consistent with NPR-A receptor is significantly increased cells cultured presence of TSH. The purpose present study was to determine whether TSH treatment, therefore, results higher levels ANF-induced intracellular cGMP, and elicits similar effects on cGMP signaling through NPR-B receptor. now show contrary expectation, long term exposure 1 mIU/ml bovine (6H medium) does not alter maximal formation. Moreover, treatment decreased C-type (CNP)-induced generation suggesting a down-regulation NPR-B. A effect ANF- CNP-induced observed FRTL precursor Scatchard analysis [ 125 I]ANF TSH-treated (6H) cultures indicated 5.6-fold increase high affinity ANF-binding sites compared TSH-deficient (5H) [binding capacity (Bmax )o f 6H 227.2 6 33.7 fmol/mg protein; Bmax 5H 40.2 4.7 protein]. mimicked by forskolin (Bu)2cAMP, indicating up-regulation via cAMP pathway. High I]CNP-binding were much lower abundance 5H, 0.80 0.06 protein), no them could be demonstrated. However, low I]CNP RT-PCR confirmed both transcripts showed NPR-B, but NPR-A. NPR-C transcript detectable medium, NPR-C. Both CNP ANF also Together data support functional change vast majority coupled production may represent novel or altered form NPR regulated independently (Endocrinology 140: 1365‐1374, 1999)