{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ramani H"],"funding":["NIA NIH HHS","NIH HHS"],"pagination":["481"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11987946"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(7)"],"pubmed_abstract":["People with HIV (PWH) have an increased risk of developing cardiovascular disease (CVD). Our recent data demonstrated that the multi-isoform proinflammatory cytokine IL-32 is upregulated in PWH and is associated with arterial stiffness and subclinical atherosclerosis. However, the mechanisms by which IL-32 contributes to the pathogenesis of these diseases remain unclear. Here, we show that while the less expressed IL-32α isoform induces the differentiation of human classical monocytes into the calcium-resorbing osteoclast cells, the dominantly expressed isoforms IL-32β and IL-32γ suppress this function through the inhibition of TGF-β and induce the differentiation of monocytes into the calcium-depositing osteocalcin+ osteoblasts. These results aligned with the increase in plasma levels of "],"journal":["Cells"],"pubmed_title":["Opposite Roles of IL-32α Versus IL-32β/γ Isoforms in Promoting Monocyte-Derived Osteoblast/Osteoclast Differentiation and Vascular Calcification in People with HIV."],"pmcid":["PMC11987946"],"funding_grant_id":["2R01AG054324-08A1","R01 AG054324"],"pubmed_authors":["Kizer JR","Sylla M","Thomas R","Jenabian MA","Durand M","Martel-Laferriere V","Tremblay CL","Ramani H","Cloutier G","Chomont N","Chartrand-Lefebvre C","Bertrand F","Landay AL","Peet MM","Ancuta P","Fortin C","Cleret-Buhot A","Trottier B","Hanna DB","Allard L","El-Far M","Sadouni M","Bunet R","Routy JP","Kaplan RC"],"additional_accession":[]},"is_claimable":false,"name":"Opposite Roles of IL-32α Versus IL-32β/γ Isoforms in Promoting Monocyte-Derived Osteoblast/Osteoclast Differentiation and Vascular Calcification in People with HIV.","description":"People with HIV (PWH) have an increased risk of developing cardiovascular disease (CVD). Our recent data demonstrated that the multi-isoform proinflammatory cytokine IL-32 is upregulated in PWH and is associated with arterial stiffness and subclinical atherosclerosis. However, the mechanisms by which IL-32 contributes to the pathogenesis of these diseases remain unclear. Here, we show that while the less expressed IL-32α isoform induces the differentiation of human classical monocytes into the calcium-resorbing osteoclast cells, the dominantly expressed isoforms IL-32β and IL-32γ suppress this function through the inhibition of TGF-β and induce the differentiation of monocytes into the calcium-depositing osteocalcin+ osteoblasts. These results aligned with the increase in plasma levels of ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2025-07-06T03:05:40.974Z","creation":"2025-07-06T03:05:40.974Z"},"accession":"S-EPMC11987946","cross_references":{"pubmed":["40214435"],"doi":["10.3390/cells14070481"]}}