ArticleArteriosclerosis, thrombosis, and vascular biology2012
Decreased Krev interaction-trapped 1 expression leads to increased vascular permeability and modifies inflammatory responses in vivo.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Rho-associated kinase inhibitors in cerebral cavernous malformations: a preclinical systematic review.Neurosurgical review · 2026Pooled it
- KRIT1 in vascular biology and beyond.Bioscience reports · 2024Review
- KRIT1: A Traffic Warden at the Busy Crossroads Between Redox Signaling and the Pathogenesis of Cerebral Cavernous Malformation Disease.Antioxidants & redox signaling · 2023Review
- KRIT1-mediated regulation of neutrophil adhesion and motility.The FEBS journal · 2023Article
- Contribution of protein-protein interactions to the endothelial-barrier-stabilizing function of KRIT1.Journal of cell science · 2022Article
- Cerebral Cavernous Malformation: Immune and Inflammatory Perspectives.Frontiers in immunology · 2022Review
- Network analysis indicating the pharmacological mechanism of Yunpi-Qufeng-Chushi-prescription in prophylactic treatment of rheumatoid arthritis.BMC complementary medicine and therapies · 2021Article
- Review
- Protein kinase Cα regulates the nucleocytoplasmic shuttling of KRIT1.Journal of cell science · 2021Article
- Cerebral Cavernous Malformation Proteins in Barrier Maintenance and Regulation.International journal of molecular sciences · 2020Review
- VEGF signalling enhances lesion burden in KRIT1 deficient mice.Journal of cellular and molecular medicine · 2020Article
- Identification of a Novel CCM1 Frameshift Mutation in a Chinese Han Family With Multiple Cerebral Cavernous Malformations.Frontiers in neuroscience · 2020Article
- Article
- KRIT1 Deficiency Promotes Aortic Endothelial Dysfunction.International journal of molecular sciences · 2019Article
- The cerebral cavernous malformation disease causing gene KRIT1 participates in intestinal epithelial barrier maintenance and regulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Multifunctional Platinum@BSA-Rapamycin Nanocarriers for the Combinatorial Therapy of Cerebral Cavernous Malformation.ACS omega · 2018Article
- Targeting therapeutics to endothelium: are we there yet?Drug delivery and translational research · 2018Review
- KRIT1 loss-of-function induces a chronic Nrf2-mediated adaptive homeostasis that sensitizes cells to oxidative stress: Implication for Cerebral Cavernous Malformation disease.Free radical biology & medicine · 2018Article
- Recent advances in cerebral cavernous malformation research.Vessel plus · 2018Article
- Up-regulation of NADPH oxidase-mediated redox signaling contributes to the loss of barrier function in KRIT1 deficient endothelium.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe regulation of vascular permeability, leukocyte trafficking, and the integrity of endothelial cell-cell contacts are closely linked by a complex mechanism of interregulation. Here, we investigate the role of Krev interaction-trapped 1 (KRIT1), an adherens junction accessory protein required for cell-cell junction stability, in regulating these vascular functions. METHODS AND
resultsKrit1(+/-) mice exhibited an enhanced edematous response to the complex inflammatory stimuli found in the passive K/BxN model of inflammatory arthritis and the murine air pouch model, yet leukocyte infiltration was unchanged. Correspondingly, reduced KRIT1 expression increased baseline arteriole and venule permeability 2-fold over that of wild-type littermates, as measured by intravital microscopy of the intact cremaster muscle vascular network, but this increase was not accompanied by increased leukocyte extravasation or activation. Direct stimulation with tumor necrosis factor-α induced increased permeability in wild-type mice, but surprisingly no increase over baseline levels was observed in Krit1(+/-) mice, despite extensive leukocyte activation. Finally, adoptive transfer of Krit1(+/-) bone marrow failed to increase permeability in wild-type mice. However, reduced expression of KRIT1 in the hematopoietic lineage dampened the differences observed in baseline permeability.
conclusionsTaken together, our data indicate an integral role for KRIT1 in microvessel homeostasis and the vascular response to inflammation.
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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.