<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>120(2)</volume><submitter>Walker EC</submitter><pubmed_abstract>Effective osteoporosis therapy requires agents that increase the amount and/or quality of bone. Any modification of osteoclast-mediated bone resorption by disease or drug treatment, however, elicits a parallel change in osteoblast-mediated bone formation because the processes are tightly coupled. Anabolic approaches now focus on uncoupling osteoblast action from osteoclast formation, for example, by inhibiting sclerostin, an inhibitor of bone formation that does not influence osteoclast differentiation. Here, we report that oncostatin M (OSM) is produced by osteoblasts and osteocytes in mouse bone and that it has distinct effects when acting through 2 different receptors, OSM receptor (OSMR) and leukemia inhibitory factor receptor (LIFR). Specifically, mouse OSM (mOSM) inhibited sclerostin</pubmed_abstract><journal>The Journal of clinical investigation</journal><pagination>582-92</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2810087</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Oncostatin M promotes bone formation independently of resorption when signaling through leukemia inhibitory factor receptor in mice.</pubmed_title><pmcid>PMC2810087</pmcid><pubmed_authors>Martin TJ</pubmed_authors><pubmed_authors>Zhang JG</pubmed_authors><pubmed_authors>Walker EC</pubmed_authors><pubmed_authors>McGregor NE</pubmed_authors><pubmed_authors>Poulton IJ</pubmed_authors><pubmed_authors>Gillespie MT</pubmed_authors><pubmed_authors>Nicola NA</pubmed_authors><pubmed_authors>Sims NA</pubmed_authors><pubmed_authors>Solano M</pubmed_authors><pubmed_authors>Constable MJ</pubmed_authors><pubmed_authors>Nicholson GC</pubmed_authors><pubmed_authors>Pompolo S</pubmed_authors><pubmed_authors>Fernandes TJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Oncostatin M promotes bone formation independently of resorption when signaling through leukemia inhibitory factor receptor in mice.</name><description>Effective osteoporosis therapy requires agents that increase the amount and/or quality of bone. Any modification of osteoclast-mediated bone resorption by disease or drug treatment, however, elicits a parallel change in osteoblast-mediated bone formation because the processes are tightly coupled. Anabolic approaches now focus on uncoupling osteoblast action from osteoclast formation, for example, by inhibiting sclerostin, an inhibitor of bone formation that does not influence osteoclast differentiation. Here, we report that oncostatin M (OSM) is produced by osteoblasts and osteocytes in mouse bone and that it has distinct effects when acting through 2 different receptors, OSM receptor (OSMR) and leukemia inhibitory factor receptor (LIFR). Specifically, mouse OSM (mOSM) inhibited sclerostin</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Feb</publication><modification>2026-03-16T17:19:09.154Z</modification><creation>2019-03-27T00:28:05Z</creation></dates><accession>S-EPMC2810087</accession><cross_references><pubmed>20051625</pubmed><doi>10.1172/JCI40568</doi><doi>10.1172/jci40568</doi></cross_references></HashMap>