ArticleThe American journal of pathology2013
β-Arrestin-1 deficiency protects mice from experimental colitis.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 40 citations in OpenAlex.
- IGF-1 protects against acute pancreatitis by suppressing NF-κB activation through the β-arrestin1/STAT3 pathway.Molecular and cellular biochemistry · 2026Article
- A novel long-galanin peptide from non-mammalian vertebrates mitigates the inflammatory response in IBD models via the biased GALR2/β-arrestin2 pathway.Nature communications · 2025Article
- A New Strategy in Modulating the Protease-Activated Receptor 2 (Par2) in Autoimmune Diseases.International journal of molecular sciences · 2025Review
- Article
- β-arrestin1 protects intestinal tight junction through promoting mitofusin 2 transcription to drive parkin-dependent mitophagy in colitis.Gastroenterology report · 2024Article
- Korean red ginseng extract prevents bone loss in an oral model of glucocorticoid induced osteoporosis in mice.Frontiers in pharmacology · 2024Article
- Ring1a protects against colitis through regulating mucosal immune system and colonic microbial ecology.Gut microbes · 2023Article
- Intersections between Copper, β-Arrestin-1, Calcium, FBXW7, CD17, Insulin Resistance and Atherogenicity Mediate Depression and Anxiety Due to Type 2 Diabetes Mellitus: A Nomothetic Network Approach.Journal of personalized medicine · 2022Article
- Loss of interleukin-10 exacerbates early Type-1 diabetes-induced bone loss.Journal of cellular physiology · 2020Article
- Beneficial effects of Lactobacillus reuteri 6475 on bone density in male mice is dependent on lymphocytes.Scientific reports · 2019Article
- Vascular Endothelial Growth Factor Receptor 3 Regulates Endothelial Function Through β-Arrestin 1.Circulation · 2019Article
- ERAP1 deficient mice have reduced Type 1 regulatory T cells and develop skeletal and intestinal features of Ankylosing Spondylitis.Scientific reports · 2018Article
- G protein-coupled receptor kinase-2-deficient mice are protected from dextran sodium sulfate-induced acute colitis.Physiological genomics · 2018Article
- Effectiveness of C5a aptamers in a TNBS-induced colitis mouse model.Experimental and therapeutic medicine · 2017Article
- Role of G protein-coupled receptor kinase-6 inPhysiological genomics · 2017Article
- Activating α7 nicotinic acetylcholine receptor inhibits NLRP3 inflammasome through regulation of β-arrestin-1.CNS neuroscience & therapeutics · 2017Article
- COX-1/PGEScientific reports · 2017Article
- Protective effect ofAmerican journal of translational research · 2017Article
- Non-Hematopoietic β-Arrestin1 Confers Protection Against Experimental Colitis.Journal of cellular physiology · 2016Article
- Multifaceted role of β-arrestins in inflammation and disease.Genes and immunity · 2015Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
β-Arrestins are intracellular scaffolding proteins that modulate specific cell signaling pathways. Recent studies, in both cell culture and in vivo models, have demonstrated an important role for β-arrestin-1 in inflammation. However, the role of β-arrestin-1 in the pathogenesis of inflammatory bowel disease (IBD) is not known. Our goal was to investigate the role of β-arrestin-1 in IBD using mouse models of colitis. To this end, we subjected wild-type (WT) and β-arrestin-1 knockout (β-arr-1(-/-)) mice to colitis induced by trinitrobenzenesulfonic acid or dextran sulfate sodium and examined the clinical signs, gross pathology, and histopathology of the colon, as well as inflammatory components. The β-arr-1(-/-) mice displayed significantly attenuated colitis, compared with WT mice, in both models. Consistent with the phenotypic observations, histological examination of the colon revealed attenuated disease pathology in the β-arr-1(-/-) mice. Our results further demonstrate that β-arr-1(-/-) mice are deficient in IL-6 expression in the colon, but have higher expression of the anti-inflammatory IL-10 family of cytokines. Our results also demonstrate diminished ERK and NFκB pathways in the colons of β-arr-1(-/-) mice, compared with WT mice. Taken together, our results demonstrate that decreased IL-6 production and enhanced IL-10 and IL-22 production in β-arrestin-1-deficient mice likely lead to attenuated gut 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.