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Increased bone density in mice lacking the proton receptor OGR1

Content Provider	Scilit
Author	Krieger, Nancy S. Yao, Zhenqiang Kyker-Snowman, Kelly Kim, Min Ho Boyce, Brendan F. Bushinsky, David A.
Copyright Year	2016
Description	Journal: Kidney International Chronic metabolic acidosis stimulates cell-mediated calcium efflux from bone through osteoblastic prostaglandin $E_{2}$-induced stimulation of receptor activator of NF-kB ligand leading to increased osteoclastic bone resorption. Osteoblasts express the proton-sensing G-protein–coupled receptor OGR1, which activates inositol phosphate–mediated intracellular calcium. Proton-induced osteoblastic intracellular calcium signaling requires ovarian cancer G-protein–coupled receptor 1 (OGR1), suggesting that OGR1 is the sensor activated during acidosis to cause bone resorption. Growing mice produce large amounts of metabolic acids, which must be buffered, primarily by bone, before excretion by the kidney. Here we tested whether lack of OGR1 inhibits proton-induced bone resorption by measuring bone mineral density by micro–computed tomography and histomorphometry in 8-week-old male $OGR1^{–/–}$ and C57/Bl6 wild type mice. $OGR1^{–/–}$ mice have normal skeletal development with no atypical gross phenotype. Trabecular and cortical bone volume was increased in tibiae and vertebrae from $OGR1^{–/–}$. There were increased osteoblast numbers on the cortical and trabecular surfaces of tibiae from $OGR1^{–/–}$ mice, increased endocortical and trabecular bone formation rates, and osteoblastic gene expression. Osteoclast numbers and surface were increased in tibiae of $OGR1^{–/–}$ mice. Thus, in rapidly growing mice, lack of OGR1 leads to increased bone mass with increased bone turnover and a greater increase in bone formation than resorption. This supports the important role of the proton receptor OGR1 in the response of bone to protons.
Related Links	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4757816/pdf http://www.kidney-international.org/article/S0085253815000940/pdf
Ending Page	573
Page Count	9
Starting Page	565
ISSN	00852538
e-ISSN	15231755
DOI	10.1016/j.kint.2015.12.020
Journal	Kidney International
Issue Number	3
Volume Number	89
Language	English
Publisher	Elsevier BV
Publisher Date	2016-01-11
Access Restriction	Open
Subject Keyword	Journal: Kidney International Metabolic Acidosis Bone Resorption Bone Formation
Content Type	Text
Resource Type	Article
Subject	Nephrology

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