ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Overexpression of Ste20-related proline/alanine-rich kinase exacerbates experimental colitis in mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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.
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
25 citing papers in PubMed, 44 citations in OpenAlex.
- The Cellular and Transcriptomic Early Innate Immune Response to BCG Vaccination in Mice.Cells · 2024Article
- Modulation of Cerebrospinal Fluid Dysregulation via a SPAK and OSR1 Targeted Framework Nucleic Acid in Hydrocephalus.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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- Article
- OXSR1 inhibits inflammasome activation by limiting potassium efflux during mycobacterial infection.Life science alliance · 2022Article
- Article
- Inflammatory hydrocephalus.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2021Article
- SPAK-p38 MAPK signal pathway modulates claudin-18 and barrier function of alveolar epithelium after hyperoxic exposure.BMC pulmonary medicine · 2021Article
- STK39 promotes breast cancer invasion and metastasis by increasing SNAI1 activity upon phosphorylation.Theranostics · 2021Article
- SPAK Deficiency Attenuates Chemotherapy-Induced Intestinal Mucositis.Frontiers in oncology · 2021Article
- STK39 is a novel kinase contributing to the progression of hepatocellular carcinoma by the PLK1/ERK signaling pathway.Theranostics · 2021Article
- Creatine Transporter, Reduced in Colon Tissues From Patients With Inflammatory Bowel Diseases, Regulates Energy Balance in Intestinal Epithelial Cells, Epithelial Integrity, and Barrier Function.Gastroenterology · 2020Article
- Fasting-Mimicking Diet Modulates Microbiota and Promotes Intestinal Regeneration to Reduce Inflammatory Bowel Disease Pathology.Cell reports · 2019Article
- WNK pathways in cancer signaling networks.Cell communication and signaling : CCS · 2018Review
- Astragaloside II promotes intestinal epithelial repair by enhancing L-arginine uptake and activating the mTOR pathway.Scientific reports · 2017Article
- Pharmacological targeting of SPAK kinase in disorders of impaired epithelial transport.Expert opinion on therapeutic targets · 2017Review
- Seawater-drowning-induced acute lung injury: From molecular mechanisms to potential treatments.Experimental and therapeutic medicine · 2017Article
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- Association of three candidate genetic variants in RAB7L1/NUCKS1, MCCC1 and STK39 with sporadic Parkinson's disease in Han Chinese.Journal of neural transmission (Vienna, Austria : 1996) · 2016Article
- Pathways to Parkinsonism Redux: convergent pathobiological mechanisms in genetics of Parkinson's disease.Human molecular genetics · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Inflammatory bowel disease, mainly Crohn's disease and ulcerative colitis, are characterized by epithelial barrier disruption and altered immune regulation. Colonic Ste20-like proline/alanine-rich kinase (SPAK) plays a role in intestinal inflammation, but its underlying mechanisms need to be defined. Both SPAK-transfected Caco2-BBE cells and villin-SPAK transgenic (TG) FVB/6 mice exhibited loss of intestinal barrier function. Further studies demonstrated that SPAK significantly increased paracellular intestinal permeability to FITC-dextran. In vivo studies using the mouse models of colitis induced by dextran sulfate sodium (DSS) and trinitrobenzene sulfonic acid showed that TG FVB/6 mice were more susceptible to DSS and trinitrobenzene sulfonic acid treatment than wild-type FVB/6 mice, as demonstrated by clinical and histological characteristics and enzymatic activities. Consistent with this notion, we found that SPAK increased intestinal epithelial permeability, which likely facilitated the production of inflammatory cytokines in vitro and in vivo, aggravated bacterial translocation in TG mice under DSS treatment, and consequently established a context favorable for the triggering of intestinal inflammation cascades. In conclusion, overexpression of SPAK inhibits maintenance of intestinal mucosal innate immune homeostasis, which makes regulation of SPAK important to attenuate pathological responses in inflammatory bowel disease.
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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.