STC1 interference on calcitonin family of receptors signaling during osteoblastogenesis via adenylate cyclase inhibition. | - CCMAR -

Journal Article

TitleSTC1 interference on calcitonin family of receptors signaling during osteoblastogenesis via adenylate cyclase inhibition.
Publication TypeJournal Article
AuthorsTerra, SR, Cardoso, JCR, Félix, RC, Martins, LAnderson M, Souza, DOnofre G, Guma, FCR, Canario, AVM, Schein, V
Year of Publication2015
JournalMol Cell Endocrinol
Volume403
Date Published2015 Mar 5
Pagination78-87
ISSN1872-8057
KeywordsAdenylyl Cyclase Inhibitors, Adenylyl Cyclases, Adipocytes, Calcitonin, Calcitonin Gene-Related Peptide, Calcitonin Receptor-Like Protein, Cell Differentiation, Cell Membrane, Colforsin, Cyclic AMP, Gene Expression Regulation, Glycoproteins, HEK293 Cells, Humans, Osteoblasts, Protein Multimerization, Receptor Activity-Modifying Protein 1, Signal Transduction, Stem Cells
Abstract

Stanniocalcin 1 (STC1) and calcitonin gene-related peptide (CGRP) are involved in bone formation/remodeling. Here we investigate the effects of STC1 on functional heterodimer complex CALCRL/RAMP1, expression and activity during osteoblastogenesis. STC1 did not modify CALCRL and ramp1 gene expression during osteoblastogenesis when compared to controls. However, plasma membrane spatial distribution of CALCRL/RAMP1 was modified in 7-day pre-osteoblasts exposed to either CGRP or STC1, and both peptides induced CALCRL and RAMP1 assembly. CGRP, but not STC1 stimulated cAMP accumulation in 7-day osteoblasts and in CALCRL/RAMP1 transfected HEK293 cells. Furthermore, STC1 inhibited forskolin stimulated cAMP accumulation of HEK293 cells, but not in CALCRL/RAMP1 transfected HEK293 cells. However, STC1 inhibited cAMP accumulation in calcitonin receptor (CTR) HEK293 transfected cells stimulated by calcitonin. In conclusion, STC1 signals through inhibitory G-protein modulates CGRP receptor spatial localization during osteoblastogenesis and may function as a regulatory factor interacting with calcitonin peptide members during bone formation.

DOI10.1016/j.mce.2015.01.010
Sapientia

http://www.ncbi.nlm.nih.gov/pubmed/25591908?dopt=Abstract

Alternate JournalMol. Cell. Endocrinol.
PubMed ID25591908
CCMAR Authors