<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Suresh S</submitter><funding>Intramural NIH HHS</funding><funding>National Institutes of Health</funding><pagination>11685-11697</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8911387</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>34(9)</volume><pubmed_abstract>Erythropoietin (EPO) regulates erythropoiesis by binding to erythropoietin receptor (Epor) on erythroid progenitor cells. Epor is also expressed on bone forming osteoblasts and bone loss accompanies EPO-stimulated erythropoiesis in mice. Mice with Epor restricted to erythroid tissue exhibit reduced bone and increased marrow adipocytes; in contrast, transgenic mice (Tg) with osteoblastic-specific deletion of Epor exhibit reduced trabecular bone with age without change in marrow adipocytes. By 12 weeks, male Tg mice had 22.2% and female Tg mice had 29.6% reduced trabecular bone volume (BV) compared to controls. EPO administration (1200 U/kg) for 10 days reduced trabecular bone in control mice but not in Tg mice. There were no differences in numbers of osteoblasts, osteoclasts, and marrow adi</pubmed_abstract><journal>FASEB journal : official publication of the Federation of American Societies for Experimental Biology</journal><pubmed_title>Erythropoietin signaling in osteoblasts is required for normal bone formation and for bone loss during erythropoietin-stimulated erythropoiesis.</pubmed_title><pmcid>PMC8911387</pmcid><funding_grant_id>ZIA DK025061</funding_grant_id><pubmed_authors>Noguchi CT</pubmed_authors><pubmed_authors>Suresh S</pubmed_authors><pubmed_authors>Lee J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Erythropoietin signaling in osteoblasts is required for normal bone formation and for bone loss during erythropoietin-stimulated erythropoiesis.</name><description>Erythropoietin (EPO) regulates erythropoiesis by binding to erythropoietin receptor (Epor) on erythroid progenitor cells. Epor is also expressed on bone forming osteoblasts and bone loss accompanies EPO-stimulated erythropoiesis in mice. Mice with Epor restricted to erythroid tissue exhibit reduced bone and increased marrow adipocytes; in contrast, transgenic mice (Tg) with osteoblastic-specific deletion of Epor exhibit reduced trabecular bone with age without change in marrow adipocytes. By 12 weeks, male Tg mice had 22.2% and female Tg mice had 29.6% reduced trabecular bone volume (BV) compared to controls. EPO administration (1200 U/kg) for 10 days reduced trabecular bone in control mice but not in Tg mice. There were no differences in numbers of osteoblasts, osteoclasts, and marrow adi</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Sep</publication><modification>2025-04-19T12:56:38.453Z</modification><creation>2025-04-19T12:56:38.453Z</creation></dates><accession>S-EPMC8911387</accession><cross_references><pubmed>32671900</pubmed><doi>10.1096/fj.202000888R</doi><doi>10.1096/fj.202000888r</doi></cross_references></HashMap>