NDLI: Osteoblastic γ-Aminobutyric Acid, Type B Receptors Negatively Regulate Osteoblastogenesis toward Disturbance of Osteoclastogenesis Mediated by Receptor Activator of Nuclear Factor κB Ligand in Mouse Bone*

Content Provider	PubMed Central
Author	Takahata, Yoshifumi Takarada, Takeshi Hinoi, Eiichi Nakamura, Yukari Fujita, Hiroyuki Yoneda, Yukio
Copyright Year	2011
Abstract	The prevailing view is that signaling machineries for the neurotransmitter GABA are also expressed by cells outside the CNS. In cultured murine calvarial osteoblasts, mRNA was constitutively expressed for both subunits 1 and 2 of metabotropic GABAB receptor (GABABR), along with inhibition by the GABABR agonist baclofen of cAMP formation, alkaline phosphatase (ALP) activity, and Ca2+ accumulation. Moreover, baclofen significantly inhibited the transactivation of receptor activator of nuclear factor-κB ligand (RANKL) gene in a manner sensitive to a GABABR antagonist, in addition to decreasing mRNA expression of bone morphogenetic protein-2 (BMP2), osteocalcin, and osterix. In osteoblastic MC3T3-E1 cells stably transfected with GABABR1 subunit, significant reductions were seen in ALP activity and Ca2+ accumulation, as well as mRNA expression of osteocalcin, osteopontin, and osterix. In cultured calvarial osteoblasts from GABABR1-null mice exhibiting low bone mineral density in tibia and femur, by contrast, both ALP activity and Ca2+ accumulation were significantly increased together with promoted expression of both mRNA and proteins for BMP2 and osterix. No significant change was seen in the number of multinucleated cells stained for tartrate-resistant acid phosphatase during the culture of osteoclasts prepared from GABABR1-null mice, whereas a significant increase was seen in the number of tartrate-resistant acid phosphatase-positive multinucleated cells in co-culture of osteoclasts with osteoblasts isolated from GABABR1-null mice. These results suggest that GABABR is predominantly expressed by osteoblasts to negatively regulate osteoblastogenesis through down-regulation of BMP2 expression toward disturbance of osteoclastogenesis after down-regulation of RANKL expression in mouse bone.
Related Links	http://dx.doi.org/10.1074/jbc.m111.253526
Ending Page	32917
Page Count	12
Starting Page	32906
File Format	PDF
ISSN	00219258
e-ISSN	1083351X
Journal	The Journal of Biological Chemistry
Issue Number	38
Volume Number	286
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2011-09-23
Access Restriction	Open
Rights Holder	American Society for Biochemistry and Molecular Biology
Subject Keyword	Cell Biology Biochemistry Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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