ArticleProceedings of the National Academy of Sciences of the United States of America2022
Splice factor polypyrimidine tract-binding protein 1 (Ptbp1) primes endothelial inflammation in atherogenic disturbed flow conditions.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- SLC15A4 promotes oral cancer progression by regulating TLR9 and activating the JAK/STAT signaling pathway.Head & face medicine · 2026Article
- Biochemical insights and microRNA profiling via next-generation sequencing in moderate and severe COVID-19 cases.Clinics (Sao Paulo, Brazil) · 2026Article
- Endothelial Elavl1 Is Required for CD8 T-Cell Persistence in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- An endothelial RNA splicing atlas catalogs effects of IL-1β and identifies an alternative PROCR isoform with genetic links to pleiotropic vascular disease.American journal of human genetics · 2026Article
- Endothelial PTBP1 Deletion in Transplanted Cardiac Tissue Limits Cardiac Allograft Vasculopathy.bioRxiv : the preprint server for biology · 2026Article
- PTBP1 supports mouse spermatogenesis by facilitating cytoskeletal organization through the mTORC2-PKCα pathway in Sertoli cells.Communications biology · 2026Article
- Beyond transcription: RNA-binding proteins steering angiogenesis.American journal of physiology. Heart and circulatory physiology · 2026Review
- Depletion of Polypyrimidine tract binding protein 1 (ptbp1) activates Müller glia-derived proliferation during zebrafish retina regeneration via modulation of the senescence secretome.Experimental eye research · 2025Article
- Raver1 linksProceedings of the National Academy of Sciences of the United States of America · 2025Article
- PIM1 instigates endothelial-to-mesenchymal transition to aggravate atherosclerosis.Theranostics · 2025Article
- Long-read proteogenomics to connect disease-associated sQTLs to the protein isoform effectors of disease.American journal of human genetics · 2024Article
- Endothelial Immunosuppression in Atherosclerosis : Translational Control by Elavl1/HuR.bioRxiv : the preprint server for biology · 2024Article
- Alternative splicing coupled to nonsense-mediated decay coordinates downregulation of non-neuronal genes in developing mouse neurons.Genome biology · 2024Article
- The role of splicing events in the inflammatory response of atherosclerosis: molecular mechanisms and modulation.Frontiers in immunology · 2024Review
- Whole-genome CRISPR screen identifies RAVER1 as a key regulator of RIPK1-mediated inflammatory cell death, PANoptosis.iScience · 2023Article
- Splice factor polypyrimidine tract-binding protein 1 (Ptbp1) primes endothelial inflammation in atherogenic disturbed flow conditions.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Exploring the Role of MicroRNAs and Associated Proteins in Multiple Sclerosis.Basic and clinical neuroscienceArticle
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
NF-κB-mediated endothelial activation drives leukocyte recruitment and atherosclerosis, in part through adhesion molecules Icam1 and Vcam1. The endothelium is primed for cytokine activation of NF-κB by exposure to low and disturbed blood flow (LDF)but the molecular underpinnings are not fully understood. In an experimental in vivo model of LDF, platelets were required for the increased expression of several RNA-binding splice factors, including polypyrimidine tract binding protein (Ptbp1). This was coordinated with changes in RNA splicing in the NF-κB pathway in primed cells, leading us to examine splice factors as mediators of priming. Using Icam1 and Vcam1 induction by tumor necrosis factor (TNF)-α stimulation as a readout, we performed a CRISPR Cas9 knockout screen and identified a requirement for Ptbp1 in priming. Deletion of Ptbp1 had no effect on cell growth or response to apoptotic stimuli, but reversed LDF splicing patterns and inhibited NF-κB nuclear translocation and transcriptional activation of downstream targets, including Icam1 and Vcam1. In human coronary arteries, elevated PTBP1 correlates with expression of TNF pathway genes and plaque. In vivo, endothelial-specific deletion of Ptbp1 reduced Icam1 expression and myeloid cell infiltration at regions of LDF in atherosclerotic mice, limiting atherosclerosis. This may be mediated, in part, by allowing inclusion of a conserved alternative exon in Ripk1 leading to a reduction in Ripk1 protein. Our data show that Ptbp1, which is induced in a subset of the endothelium by platelet recruitment at regions of LDF, is required for priming of the endothelium for subsequent NF-κB activation, myeloid cell recruitment and atherosclerosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.