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RNA interference of the BMPR‐IB gene blocks BMP‐2‐induced osteogenic gene expression in human bone cells
Author(s) -
Singhatanadgit W.,
Salih V.,
Olsen I.
Publication year - 2008
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2008.08.005
Subject(s) - gene knockdown , transfection , osteocalcin , osteoblast , microbiology and biotechnology , bone morphogenetic protein , bone morphogenetic protein receptor , biology , bone morphogenetic protein 2 , alkaline phosphatase , chemistry , cell culture , gene , in vitro , biochemistry , genetics , enzyme
We have previously shown that human bone cells express bone morphogenetic protein receptor‐IB (BMPR‐IB). However, little is known about the precise role of this receptor in the response of osteoblastic genes to the BMP in these cells. To determine BMPR‐IB‐dependent osteoblastic gene expression, the present study examined the effects of BMPR‐IB knockdown on BMP‐induced osteoblast‐associated genes. BMPR‐IB mRNA and protein were markedly suppressed by transfection of cells with BMPR‐IB siRNA. Using three different bone cell samples, BMP‐2 stimulation of alkaline phosphatase (ALP), osteocalcin (OC), distal‐less homeobox‐5 (Dlx5) and core binding factor alpha‐1 (Cbfa1) was found to be specifically and significantly reduced in the BMPR‐IB siRNA‐transfected cultures compared with that of control cultures. Our study has provided evidence that BMPR‐IB‐dependent signaling plays a crucial role in BMP‐2 up‐regulation of the ALP, OC, Dlx5 and Cbfa1 genes in bone cells, suggesting a pivotal role of this receptor in BMP‐2‐induced osteoblast differentiation in vitro . These findings thus suggest the possibility that BMPR‐IB could be a therapeutic target for enhancing bone regeneration in vivo .