ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2022
RNF213 loss of function reshapes vascular transcriptome and spliceosome leading to disrupted angiogenesis and aggravated vascular inflammatory responses.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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21 citing papers in PubMed, 23 citations in OpenAlex.
- Multiomics profiling and experiments in preclinical models revealed RAD51-IN-1 as a synergistic potentiator of anlotinib sensitivity.Science advances · 2026Trial
- Lipid metabolism in moyamoya disease: Emerging evidence, vascular remodeling, and therapeutic implications.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Review
- RNF213 in Panvascular Disease: A Molecular Hub Linking Genetic Susceptibility to Systemic Vasculopathy.Biomedicines · 2026Review
- Engineering etiology-aligned in vitro models of human vessels.Microsystems & nanoengineering · 2026Review
- MicroRNA-29b-3p promotes endothelial cell inflammation via NTRK2/PI3K/NLRP3 pathway in Moyamoya disease.European journal of medical research · 2025Article
- RNF213 Knockdown and Inflammation Promote Angiogenesis and Phenotype Switching by JAK2/STAT3 Pathway in Moyamoya Disease.Molecular neurobiology · 2025Article
- The multifaceted role of RNF213 in oncogenesis: current insights and future research directions.Discover oncology · 2025Review
- Multisystemic Impact of RNF213 Arg4810Lys: A Comprehensive Review of Moyamoya Disease and Associated Vasculopathies.International journal of molecular sciences · 2025Review
- Association of alterations in transcriptomics and intestinal immune responses with Bifidobacterium longum BAA2573 in improving dextran sulfate sodium-induced colitis.BMC gastroenterology · 2025Article
- Integrative molecular subtyping and diagnostic model construction for Moyamoya disease based on diverse programmed cell death gene patterns.Orphanet journal of rare diseases · 2025Article
- Recent Advances in Genetics of Moyamoya Disease: Insights into the Different Pathogenic Pathways.International journal of molecular sciences · 2025Review
- Characterization of moyamoya disease molecular subtypes through disulfidptosis‑related genes and immune landscape analysis.Experimental and therapeutic medicine · 2025Article
- The Role of Immune Cells in Moyamoya Disease.Brain sciences · 2025Review
- Identification of key regulators in pancreatic ductal adenocarcinoma using network theoretical approach.PloS one · 2025Article
- ExploringBiomedicines · 2024Review
- CXCL12/CXCR4 pathway as a novel therapeutic target for RNF213-associated pulmonary arterial hypertension.Scientific reports · 2024Article
- Circulating immune cell landscape and T-cell abnormalities in patients with moyamoya disease.Clinical and translational medicine · 2024Article
- Physiological and pathophysiological mechanisms of the molecular and cellular biology of angiogenesis and inflammation in moyamoya angiopathy and related vascular diseases.Frontiers in neurology · 2023Review
- Clinical value of the systemic immune-inflammation index in moyamoya disease.Frontiers in neurology · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RNF213 gene mutations are the cause behind Moyamoya disease, a rare cerebrovascular occlusive disease. However, the function of RNF213 in the vascular system and the impact of its loss of function are not yet comprehended. To understand RNF23 function, we performed gene knockdown (KD) in vascular cells and performed various phenotypical analysis as well as extensive transcriptome and epitranscriptome profiling. Our data revealed that RNF213 KD led to disrupted angiogenesis in HUVEC, in part due to downregulation of DNA replication and proliferation pathways. Furthermore, HUVEC cells became sensitive to LPS induced inflammation after RNF213 KD, leading to retarded cell migration and enhanced macrophage transmigration. This was evident at the level of transcriptome as well. Interestingly, RNF213 led to extensive changes in mRNA splicing that were not previously reported. In vascular smooth muscle cells (vSMCs), RNF213 KD led to alteration in cytoskeletal organization, contractility, and vSMCs function related pathways. Finally, RNF213 KD disrupted endothelial-to-vSMCs communication in co-culture models. Overall, our results indicate that RNF213 KD sensitizes endothelial cells to inflammation, leading to altered angiogenesis. Our results shed the light on the important links between RNF213 mutations and inflammatory/immune inducers of MMD and on the unexplored role of epitranscriptome in MMD.
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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.