ArticleThe American journal of pathology2008
Hyaluronan-mediated leukocyte adhesion and dextran sulfate sodium-induced colitis are attenuated in the absence of signal transducer and activator of transcription 1.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- OTUD5 maintains STAT1/2 stability and promotes IFNγ-driven intestinal inflammation.The Journal of biological chemistry · 2026Article
- STAT1 mediates the pro-inflammatory role of GBP5 in colitis.Communications biology · 2025Article
- Discovery of a dual-acting inhibitor of interleukin-1β and STATs for the treatment of inflammatory bowel disease.RSC medicinal chemistry · 2024Article
- STAT1-mediated induction of Ly6c-expressing macrophages are involved in the pathogenesis of an acute colitis model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Gut-associated cGMP mediates colitis and dysbiosis in a mouse model of an activating mutation in GUCY2C.The Journal of experimental medicine · 2021Article
- Astragaloside IV Alleviates the Experimental DSS-Induced Colitis by Remodeling Macrophage Polarization Through STAT Signaling.Frontiers in immunology · 2021Article
- The Inter-α-Trypsin Inhibitor Family: Versatile Molecules in Biology and Pathology.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- Differential regulation of JAK/STAT-signaling in patients with ulcerative colitis and Crohn's disease.World journal of gastroenterology · 2020Review
- JAK-STAT pathway targeting for the treatment of inflammatory bowel disease.Nature reviews. Gastroenterology & hepatology · 2020Review
- Article
- Damage-associated molecular patterns in inflammatory bowel disease: From biomarkers to therapeutic targets.World journal of gastroenterology · 2018Review
- Deficiency in STAT1 Signaling Predisposes Gut Inflammation and Prompts Colorectal Cancer Development.Cancers · 2018Article
- STAT1 is a sex-specific tumor suppressor in colitis-associated colorectal cancer.Molecular oncology · 2018Article
- A novel method for crosstalk analysis of biological networks: improving accuracy of pathway annotation.Nucleic acids research · 2017Article
- Integrating Immunologic Signaling Networks: The JAK/STAT Pathway in Colitis and Colitis-Associated Cancer.Vaccines · 2016Review
- Hyaluronan as a therapeutic target in human diseases.Advanced drug delivery reviews · 2016Review
- The role of hyaluronan in innate defense responses of the intestine.International journal of cell biology · 2015Review
- Expression of versican V3 by arterial smooth muscle cells alters tumor growth factor β (TGFβ)-, epidermal growth factor (EGF)-, and nuclear factor κB (NFκB)-dependent signaling pathways, creating a microenvironment that resists monocyte adhesion.The Journal of biological chemistry · 2014Article
- Hyaluronan, a crucial regulator of inflammation.Frontiers in immunology · 2014Review
- Lacritin-induced secretion of tear proteins from cultured monkey lacrimal acinar cells.Investigative ophthalmology & visual science · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Inflammatory bowel disease is a chronic inflammatory condition of the intestinal mucosa whose etiology is unclear but is likely to be multifactorial. We have shown previously that an increased amount of hyaluronan (HA) is present both in the inflamed mucosa of inflammatory bowel disease patients and in isolated human cells after polyI:C treatment. The signal transducer and activator of transcription (STAT)1 protein plays an important role in many signaling pathways that are associated with inflammation. We therefore investigated the role of STAT1 in adhesive interactions that occur between leukocytes and polyI:C-induced mucosal smooth muscle cells (M-SMCs). Activation of STAT1 was observed after the polyI:C treatment of M-SMCs. Specific phosphorylation of tyrosine and serine residues of STAT1 was observed in polyI:C-treated, but not untreated, M-SMC cultures. To evaluate further the role of STAT1, a corresponding STAT-1-null mouse was used. PolyI:C-induced, HA-mediated leukocyte adhesion to colon SMCs from STAT1-null mice was significantly decreased compared with that from wild-type control mice. In vivo, using the dextran sulfate sodium-induced model of colon inflammation, both tissue damage and HA deposition were attenuated in STAT1-null mice compared with that in wild-type control mice. Additionally, the inter-alpha-trypsin inhibitor (IalphaI), a proteoglycan essential for facilitating leukocyte binding to the HA matrix, was reduced in STAT1-null mice. Together, these results demonstrate that STAT1 plays an important role in HA-mediated inflammatory processes.
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Registered trials
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