ArticleJournal of immunology (Baltimore, Md. : 1950)2019
The GTPase Rab1 Is Required for NLRP3 Inflammasome Activation and Inflammatory Lung Injury.
Article in Journal of immunology (Baltimore, Md. : 1950), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
- Singapore grouper iridovirus utilizes Rab1 to facilitate viral trafficking and evade the immune response by targeting the STING-IRF3 pathway.Cell communication and signaling : CCS · 2025Article
- The role of abnormal epigenetic regulation of small GTPases in glioma (Review).International journal of oncology · 2025Review
- C118P Suppresses Gastric Cancer Growth via Promoting Autophagy-Lysosomal Degradation of RAB1A.Pharmaceutics · 2024Article
- A dual role of ERGIC-localized Rabs in TMED10-mediated unconventional protein secretion.Nature cell biology · 2024Article
- Deciphering the molecular regulatory of RAB32/GPRC5A axis in chronic obstructive pulmonary disease.Respiratory research · 2024Article
- Mapping Research Trends and Hotspots in the Link between Alzheimer's Disease and Gut Microbes over the Past Decade: A Bibliometric Analysis.Nutrients · 2023Review
- Long noncoding RNA signatures in intrauterine infection/inflammation-induced lung injury: an integrative bioinformatics study.BMC pulmonary medicine · 2023Article
- p120-Catenin suppresses NLRP3 inflammasome activation in macrophages.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Article
- Targeted disruption of Rab1a causes early embryonic lethality.International journal of molecular medicine · 2022Article
- Surfactant Protein A Enhances the Degradation of LPS-Induced TLR4 in Primary Alveolar Macrophages Involving Rab7, β-arrestin2, and mTORC1.Infection and immunity · 2022Article
- The role of the Siglec-G ITIM domain during bacterial infection.Cellular and molecular biology (Noisy-le-Grand, France) · 2022Article
- Targeting Small GTPases and Their Prenylation in Diabetes Mellitus.Journal of medicinal chemistry · 2021Review
- Nlrp3 Deficiency Alleviates Angiotensin II-Induced Cardiomyopathy by Inhibiting Mitochondrial Dysfunction.Oxidative medicine and cellular longevity · 2021Article
- Exosome-inflammasome crosstalk and their roles in inflammatory responses.Theranostics · 2021Review
- Activation of NLRP3 Inflammasome and Onset of Alzheimer's Disease.Frontiers in immunology · 2021Review
- MicroRNA-3613-5p Promotes Lung Adenocarcinoma Cell Proliferation through a RELA and AKT/MAPK Positive Feedback Loop.Molecular therapy. Nucleic acids · 2020Article
- MiR-1202 Exerts Neuroprotective Effects on OGD/R Induced Inflammation in HM Cell by Negatively Regulating Rab1a Involved in TLR4/NF-κB Signaling Pathway.Neurochemical research · 2020Article
- Pro-inflammatory role of NLRP3 inflammasome in experimental sterile corneal inflammation.Scientific reports · 2019Article
- Mechanism of Incisional Pain: Novel Finding on Long Noncoding RNA XIST/miR-340-5p/RAB1A Axis.ASN neuroArticle
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Uncontrolled inflammatory response during sepsis predominantly contributes to the development of multiorgan failure and lethality. However, the cellular and molecular mechanisms for excessive production and release of proinflammatory cytokines are not clearly defined. In this study, we show the crucial role of the GTPase Ras-related protein in brain (Rab)1a in regulating the nucleotide binding domain-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome activation and lung inflammatory injury. Expression of dominant negative Rab1 N124I plasmid in bone marrow-derived macrophages prevented the release of IL-1β and IL-18, NLRP3 inflammasome activation, production of pro-IL-1β and pro-IL-18, and attenuated TLR4 surface expression and NF-кB activation induced by bacterial LPS and ATP compared with control cells. In alveolar macrophage-depleted mice challenged with cecal ligation and puncture, pulmonary transplantation of Rab1a-inactivated macrophages by expression of Rab1 N124I plasmid dramatically reduced the release of IL-1β and IL-18, neutrophil count in bronchoalveolar lavage fluid, and inflammatory lung injury. Rab1a activity was elevated in alveolar macrophages from septic patients and positively associated with severity of sepsis and respiratory dysfunction. Thus, inhibition of Rab1a activity in macrophages resulting in the suppression of NLRP3 inflammasome activation may be a promising target for the treatment of patients with sepsis.
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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.