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A Distinct Cation‐Sensing Mechanism in MC3T3‐E1 Osteoblasts Functionally Related to the Calcium Receptor
Author(s) -
Quarles L. Darryl,
Hartle James E.,
Siddhanti Suresh R.,
Guo Rong,
Hinson Todd K.
Publication year - 1997
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1359/jbmr.1997.12.3.393
Subject(s) - osteoblast , chemistry , transfection , calcium , luciferase , microbiology and biotechnology , receptor , extracellular , osteocalcin , biochemistry , biology , alkaline phosphatase , in vitro , gene , enzyme , organic chemistry
The presence of a cation‐sensing mechanism in osteoblasts is suggested by the ability of specific cations to stimulate osteoblastic proliferation in culture and to induce de novo bone formation in some experimental models. Our study examines whether extracellular cations stimulate osteoblasts through the recently identified G protein–coupled calcium receptor (CaR). We found that CaR agonists, calcium (Ca 2+ ), gadolinium (Gd 3+ ), aluminum (Al 3+ ), and neomycin, stimulated DNA synthesis in murine‐derived MC3T3‐E1 preosteoblasts, whereas magnesium (Mg 2+ ), nickel (Ni 2+ ), cadmium (Cd 2+ ), and zinc (Zn 2+ ) had no effect. With the exception of Mg 2+ , the cation specificities and apparent affinities were similar to that reported for CaR. CaR agonists also stimulated DNA synthesis in C3HT10 1/2 fibroblasts, but not in mesangial PVG, CHO, hepatic HTC, COS‐7 cells, or malignant transformed ROS17/2.8 and UMR‐106 osteoblasts. In addition, similar to other growth factors, CaR agonists activated transcription of a serum response element luciferase reporter construct (SRE‐Luc) stably transfected into MC3T3‐E1 osteoblasts, but had no effect on SRE‐Luc transfected into CHO and COS‐7 cells. We were unable to detect CaR expression by Northern analysis using a mouse CaR‐specific probe or to amplify CaR mRNA by reverse transcribed polymerase chain reaction in MC3T3‐E1 osteoblasts. These findings suggest that an extracellular cation‐sensing mechanism is present in murine‐derived osteoblasts that is functionally similar to but molecularly distinct from CaR.