<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kolind M</submitter><funding>Perpetual Foundation</funding><funding>Ramaciotti Foundation</funding><funding>Cancer Institute New South Wales Research Equipment</funding><funding>NHMRC</funding><funding>NIH/NIAMS</funding><funding>Sydney Medical School Research Infrastructure Major Equipment Scheme</funding><funding>NIAMS NIH HHS</funding><funding>Ian Potter Foundation</funding><funding>Australian National Health and Medical Research Council</funding><pagination>53-59</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4844190</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>81</volume><pubmed_abstract>To better understand the relative contributions of mesenchymal and endothelial progenitor cells to rhBMP-2 induced bone formation, we examined the distribution of lineage-labeled cells in Tie2-Cre:Ai9 and αSMA-creERT2:Col2.3-GFP:Ai9 reporter mice. Established orthopedic models of ectopic bone formation in the hind limb and spine fusion were employed. Tie2-lineage cells were found extensively in the ectopic bone and spine fusion masses, but co-staining was only seen with tartrate-resistant acid phosphatase (TRAP) activity (osteoclasts) and CD31 immunohistochemistry (vascular endothelial cells), and not alkaline phosphatase (AP) activity (osteoblasts). To further confirm the lack of a functional contribution of Tie2-lineage cells to BMP-induced bone, we developed conditional knockout mice wh</pubmed_abstract><journal>Bone</journal><pubmed_title>Lineage tracking of mesenchymal and endothelial progenitors in BMP-induced bone formation.</pubmed_title><pmcid>PMC4844190</pmcid><funding_grant_id>20100508</funding_grant_id><funding_grant_id>730</funding_grant_id><funding_grant_id>APP1003480</funding_grant_id><funding_grant_id>R01 AR055607</funding_grant_id><funding_grant_id>10/REG/1-23</funding_grant_id><funding_grant_id>AR055607</funding_grant_id><funding_grant_id>3037/2010</funding_grant_id><funding_grant_id>2009-02759</funding_grant_id><funding_grant_id>APP1003478</funding_grant_id><pubmed_authors>Schindeler A</pubmed_authors><pubmed_authors>Matthews BG</pubmed_authors><pubmed_authors>Kolind M</pubmed_authors><pubmed_authors>Bobyn JD</pubmed_authors><pubmed_authors>Aiken A</pubmed_authors><pubmed_authors>Kalajzic I</pubmed_authors><pubmed_authors>Mikulec K</pubmed_authors><pubmed_authors>Little DG</pubmed_authors></additional><is_claimable>false</is_claimable><name>Lineage tracking of mesenchymal and endothelial progenitors in BMP-induced bone formation.</name><description>To better understand the relative contributions of mesenchymal and endothelial progenitor cells to rhBMP-2 induced bone formation, we examined the distribution of lineage-labeled cells in Tie2-Cre:Ai9 and αSMA-creERT2:Col2.3-GFP:Ai9 reporter mice. Established orthopedic models of ectopic bone formation in the hind limb and spine fusion were employed. Tie2-lineage cells were found extensively in the ectopic bone and spine fusion masses, but co-staining was only seen with tartrate-resistant acid phosphatase (TRAP) activity (osteoclasts) and CD31 immunohistochemistry (vascular endothelial cells), and not alkaline phosphatase (AP) activity (osteoblasts). To further confirm the lack of a functional contribution of Tie2-lineage cells to BMP-induced bone, we developed conditional knockout mice wh</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Dec</publication><modification>2025-04-29T10:12:57.28Z</modification><creation>2019-03-27T02:12:21Z</creation></dates><accession>S-EPMC4844190</accession><cross_references><pubmed>26141839</pubmed><doi>10.1016/j.bone.2015.06.023</doi></cross_references></HashMap>