Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1016/j.kint.2015.12.020 http://scihub22266oqcxt.onion/10.1016/j.kint.2015.12.020 C4757816!4757816!26880453     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Kidney+Int 2016 ; 89 (3): 565-73 Nephropedia Template TP {{tp|p=26880453|t=2016. Increased bone density in mice lacking the proton receptor, OGR1 |pdf=|usr=}}{{26880453}} gab.com Text Increased bone density in mice lacking the proton receptor, OGR1 JO: Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=26880453 #FOAvip Chronic metabolic acidosis stimulates cell-mediated calcium efflux from bone through osteoblastic prostaglandin E2-induced stimulation of RANKL leading to increased osteoclastic bone resorption. Osteoblasts express the proton-sensing G-protein coupled receptor, OGR1, which activates IP3-mediated intracellular calcium. Proton-induced osteoblastic intracellular calcium signaling requires OGR1, suggesting 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, prior to excretion by the kidney. Here we tested whether lack of OGR1 inhibits proton-induced bone resorption by measuring bone mineral density by ?CT 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. Twit Text FOAVip Increased bone density in mice lacking the proton receptor, OGR1 ????Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=26880453 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26880453 #FOAvip English Wikipedia <ref>{{Cite pmid|26880453}}</ref> Increased bone density in mice lacking the proton receptor, OGR1 #MMPMID26880453 Krieger NS; Yao Z; Kyker-Snowman K; Kim MH; Boyce BF; Bushinsky DA Kidney Int 2016[Mar]; 89 (3): 565-73 PMID26880453show ga Chronic metabolic acidosis stimulates cell-mediated calcium efflux from bone through osteoblastic prostaglandin E2-induced stimulation of RANKL leading to increased osteoclastic bone resorption. Osteoblasts express the proton-sensing G-protein coupled receptor, OGR1, which activates IP3-mediated intracellular calcium. Proton-induced osteoblastic intracellular calcium signaling requires OGR1, suggesting 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, prior to excretion by the kidney. Here we tested whether lack of OGR1 inhibits proton-induced bone resorption by measuring bone mineral density by ?CT 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. äIncreased bone density in mice lacking the proton receptor, OGR1 (epmc).pdf DeepDyve Pubget Overpricing