ArticleThe Journal of experimental medicine2014
Targeting PI3Kγ activity decreases vascular trauma-induced intimal hyperplasia through modulation of the Th1 response.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- IRF5 governs macrophage adventitial infiltration to fuel abdominal aortic aneurysm formation.JCI insight · 2024Article
- Screening of potential regulatory genes in carotid atherosclerosis vascular immune microenvironment.PloS one · 2024Article
- A minor tweak in transplant surgery protocols alters the cellular landscape of the arterial wall during transplant vasculopathy.Frontiers in transplantation · 2024Article
- Mast cell activation and degranulation in acute artery injury: A target for post-operative therapy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- The role of PI3Kγ in the immune system: new insights and translational implications.Nature reviews. Immunology · 2022Review
- PI3K Isoforms in Vascular Biology, A Focus on the Vascular System-Immune Response Connection.Current topics in microbiology and immunology · 2022Article
- MicroRNA-146b-3p regulates the dysfunction of vascular smooth muscle cells via repressing phosphoinositide-3 kinase catalytic subunit gamma.Bioengineered · 2021Article
- Article
- Phosphoinositide Signaling and Mechanotransduction in Cardiovascular Biology and Disease.Frontiers in cell and developmental biology · 2020Review
- Function, Regulation and Biological Roles of PI3Kγ Variants.Biomolecules · 2019Review
- A class of highly selective inhibitors bind to an active state of PI3Kγ.Nature chemical biology · 2019Article
- PI3Kγ (Phosphoinositide 3-Kinase γ) Regulates Vascular Smooth Muscle Cell Phenotypic Modulation and Neointimal Formation Through CREB (Cyclic AMP-Response Element Binding Protein)/YAP (Yes-Associated Protein) Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Immune and Smooth Muscle Cells Interactions in Atherosclerosis: How to Target a Breaking Bad Dialogue?Frontiers in pharmacology · 2019Review
- PI3Kγ promotes vascular smooth muscle cell phenotypic modulation and transplant arteriosclerosis via a SOX9-dependent mechanism.EBioMedicine · 2018Article
- Involvement of CD8+ T cell subsets in early response to vascular injury in patients with peripheral artery disease in vivo.Clinical immunology (Orlando, Fla.) · 2018Article
- Inhibition of p110δ PI3K prevents inflammatory response and restenosis after artery injury.Bioscience reports · 2017Article
- Evolutionary history of phosphatidylinositol- 3-kinases: ancestral origin in eukaryotes and complex duplication patterns.BMC evolutionary biology · 2015Article
- The Activation Function-1 of Estrogen Receptor Alpha Prevents Arterial Neointima Development Through a Direct Effect on Smooth Muscle Cells.Circulation research · 2015Article
- Article
- Platelet PI3Kγ Contributes to Carotid Intima-Media Thickening under Severely Reduced Flow Conditions.PloS one · 2015Article
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interventional strategies to treat atherosclerosis, such as transluminal angioplasty and stent implantation, often cause vascular injury. This leads to intimal hyperplasia (IH) formation that induces inflammatory and fibroproliferative processes and ultimately restenosis. We show that phosphoinositide 3-kinase γ (PI3Kγ) is a key player in IH formation and is a valid therapeutic target in its prevention/treatment. PI3Kγ-deficient mice and mice expressing catalytically inactive PI3Kγ (PI3Kγ KD) showed reduced arterial occlusion and accumulation of monocytes and T cells around sites of vascular lesion. The transfer of PI3Kγ KD CD4(+) T cells into Rag2-deficient mice greatly reduced vascular occlusion compared with WT cells, clearly demonstrating the involvement of PI3Kγ in CD4(+) T cells during IH formation. In addition we found that IH is associated with increased levels of Th1 and Th17 cytokines. A specific decrease in the Th1 response was observed in the absence of PI3Kγ activity, leading to decreased CXCL10 and RANTES production by smooth muscle cells. Finally, we show that treatment with the PI3Kγ inhibitor AS-605240 is sufficient to decrease IH in both mouse and rat models, reinforcing the therapeutic potential of PI3Kγ inhibition. Altogether, these findings demonstrate a new role for PI3Kγ activity in Th1-controlled IH development.
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