Nicotine and CRLR mRNA expression in MC3T3-E1 osteoblasts

Objective: To determine if nicotine impacts expression of CRLR mRNA in murine osteoblastic MC3T3-E1 cells. Background: Osteoblasts are central players in bone remodeling, regulating both anabolic and catabolic processes. One mediator of osteoblast function is calcitonin gene related peptide (CGRP), a bone active neuropeptide that exerts its effects via a membrane surface receptor known as the calcitonin receptor like receptor (CRLR). Because variation in CRLR expression may modify a cell's sensitivity to, and signaling capacity for, CGRP, previous experiments using human MG-63 osteoblast-like cells were conducted to determine if mediators known to impact bone health may potentially exert their regulating influence via the CGRP/CRLR signaling pathway. In this regard, nicotine, a tobacco component thought to mediate some of the detrimental actions of tobacco on bone, was found to decrease CRLR mRNA expression and CGRP-induced protein kinase A activation in MG-63 cells. Methods: MC3T3-E1 osteoblastic cells were exposed to nicotine for four hours at concentrations relevant to smoking and oral tobacco usage. Total RNA was harvested and CRLR mRNA expression was assessed by standardized RT-PCR indexed to β-actin. Results: Nicotine suppressed CRLR mRNA expression in MC3T3-E1 cells in a manner similar to that observed previously using human MG-63 osteosarcoma cells. Conclusion: Nicotine exposure suppressed CRLR mRNA expression in murine MC3T3-E1 osteoblastic cells.