{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hilt ZT"],"funding":["NCATS NIH HHS","NHLBI NIH HHS","NIH"],"pagination":["655-669"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8319031"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["128(5)"],"pubmed_abstract":["<h4>Rationale</h4>Circulating monocytes can have proinflammatory or proreparative phenotypes. The endogenous signaling molecules and pathways that regulate monocyte polarization in vivo are poorly understood. We have shown that platelet-derived β2M (β-2 microglobulin) and TGF-β (transforming growth factor β) have opposing effects on monocytes by inducing inflammatory and reparative phenotypes, respectively, but each bind and signal through the same receptor. We now define the signaling pathways involved.<h4>Objective</h4>To determine the molecular mechanisms and signal transduction pathways by which β2M and TGF-β regulate monocyte responses both in vitro and in vivo.<h4>Methods and results</h4>Wild-type- (WT) and platelet-specific β2M knockout mice were treated intravenously with either β2"],"journal":["Circulation research"],"pubmed_title":["β2M Signals Monocytes Through Non-Canonical TGFβ Receptor Signal Transduction."],"pmcid":["PMC8319031"],"funding_grant_id":["UL1 TR002001","R01 HL138673","R01 HL142152","HL142152","HL153409-01","HL141106-01A1","R01 HL141106"],"pubmed_authors":["Tesoro L","Ture SK","Pariser DN","Morrell CN","Hilt ZT","Maurya P","McGrath KE","Cleary SJ","Looney MR"],"additional_accession":[]},"is_claimable":false,"name":"β2M Signals Monocytes Through Non-Canonical TGFβ Receptor Signal Transduction.","description":"<h4>Rationale</h4>Circulating monocytes can have proinflammatory or proreparative phenotypes. The endogenous signaling molecules and pathways that regulate monocyte polarization in vivo are poorly understood. We have shown that platelet-derived β2M (β-2 microglobulin) and TGF-β (transforming growth factor β) have opposing effects on monocytes by inducing inflammatory and reparative phenotypes, respectively, but each bind and signal through the same receptor. We now define the signaling pathways involved.<h4>Objective</h4>To determine the molecular mechanisms and signal transduction pathways by which β2M and TGF-β regulate monocyte responses both in vitro and in vivo.<h4>Methods and results</h4>Wild-type- (WT) and platelet-specific β2M knockout mice were treated intravenously with either β2","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Mar","modification":"2025-04-19T12:52:28.871Z","creation":"2025-04-19T12:52:28.871Z"},"accession":"S-EPMC8319031","cross_references":{"pubmed":["33508948"],"doi":["10.1161/CIRCRESAHA.120.317119","10.1161/circresaha.120.317119"]}}