<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Jones FK</submitter><funding>Wellcome Trust ISSF</funding><funding>Oswestry Rheumatology Association</funding><funding>School of Medicine, Keele University</funding><funding>UK EPSRC/MRC CDT</funding><funding>BBSRC-DTP</funding><pagination>20487</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7686503</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(1)</volume><pubmed_abstract>Rheumatoid arthritis (RA) is a debilitating and painful inflammatory autoimmune disease characterised by the accumulation of leukocytes in the synovium, cartilage destruction and bone erosion. The immunomodulatory effects of bone marrow derived mesenchymal stem cells (MSCs) has been widely studied and the recent observations that syndecan-3 (SDC3) is selectively pro-inflammatory in the joint led us to hypothesise that SDC3 might play an important role in MSC biology. MSCs isolated from bone marrow of wild type and Sdc3&lt;sup>-/-&lt;/sup> mice were used to assess immunophenotype, differentiation, adhesion and migration properties and cell signalling pathways. While both cell types show similar differentiation potential and forward scatter values, the cell complexity in wild type MSCs was signifi</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Syndecan-3 regulates MSC adhesion, ERK and AKT signalling in vitro and its deletion enhances MSC efficacy in a model of inflammatory arthritis in vivo.</pubmed_title><pmcid>PMC7686503</pmcid><funding_grant_id>EP/F500491/1</funding_grant_id><pubmed_authors>Forsyth NR</pubmed_authors><pubmed_authors>Hyland M</pubmed_authors><pubmed_authors>Stefan A</pubmed_authors><pubmed_authors>Morgan R</pubmed_authors><pubmed_authors>Kehoe O</pubmed_authors><pubmed_authors>Kay AG</pubmed_authors><pubmed_authors>Jones FK</pubmed_authors><pubmed_authors>Pisconti A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Syndecan-3 regulates MSC adhesion, ERK and AKT signalling in vitro and its deletion enhances MSC efficacy in a model of inflammatory arthritis in vivo.</name><description>Rheumatoid arthritis (RA) is a debilitating and painful inflammatory autoimmune disease characterised by the accumulation of leukocytes in the synovium, cartilage destruction and bone erosion. The immunomodulatory effects of bone marrow derived mesenchymal stem cells (MSCs) has been widely studied and the recent observations that syndecan-3 (SDC3) is selectively pro-inflammatory in the joint led us to hypothesise that SDC3 might play an important role in MSC biology. MSCs isolated from bone marrow of wild type and Sdc3&lt;sup>-/-&lt;/sup> mice were used to assess immunophenotype, differentiation, adhesion and migration properties and cell signalling pathways. While both cell types show similar differentiation potential and forward scatter values, the cell complexity in wild type MSCs was signifi</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Nov</publication><modification>2025-04-27T02:54:15.972Z</modification><creation>2021-02-20T00:26:54Z</creation></dates><accession>S-EPMC7686503</accession><cross_references><pubmed>33235244</pubmed><doi>10.1038/s41598-020-77514-z</doi></cross_references></HashMap>