ArticleGastroenterology2012
Increased levels of survivin, via association with heat shock protein 90, in mucosal T cells from patients with Crohn's disease.
Article in Gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 31 citations in OpenAlex.
- Survivin Impairs the Apoptotic Machinery in CD4+ T Cells of Patients with Ulcerative Colitis.Journal of innate immunity · 2020Trial
- Decreased gene expression of interleukin 2 receptor subunit γ (CD132) in tissues of patients with Crohn's disease.World journal of gastroenterology · 2025Article
- Dysregulation of Survivin-Targeting microRNAs in Autoimmune Diseases: New Perspectives for Novel Therapies.Frontiers in immunology · 2022Review
- Gatekeepers of the Gut: The Roles of Proteasomes at the Gastrointestinal Barrier.Biomolecules · 2021Review
- Emerging Pathological Engagement of Ferroptosis in Gut Diseases.Oxidative medicine and cellular longevity · 2021Review
- Ablation of Survivin in T Cells Attenuates Acute Allograft Rejection after Murine Heterotopic Heart Transplantation by Inducing Apoptosis.Frontiers in immunology · 2021Article
- Survivin Promotes Piperlongumine Resistance in Ovarian Cancer.Frontiers in oncology · 2019Article
- Peripheral Lymphocytes of Patients with Inflammatory Bowel Disease Have Altered Concentrations of Key Apoptosis Players: Preliminary Results.BioMed research international · 2018Article
- Survivin expression pattern in the intestine of normoxic and ischemic rats.BMC gastroenterology · 2017Article
- Gastrointestinal and Hepatic Complications of Immune Checkpoint Inhibitors.Current gastroenterology reports · 2017Review
- Epithelial PIK3R1 (p85) and TP53 Regulate Survivin Expression during Adaptation to Ileocecal Resection.The American journal of pathology · 2016Article
- Immunopathogenesis of IBD: current state of the art.Nature reviews. Gastroenterology & hepatology · 2016Review
- Suppressed diversity of survivin splicing in active rheumatoid arthritis.Arthritis research & therapy · 2015Article
- Cell death and inflammatory bowel diseases: apoptosis, necrosis, and autophagy in the intestinal epithelium.BioMed research international · 2014Review
- Exploring dendritic cell based vaccines targeting survivin for the treatment of head and neck cancer patients.Journal of translational medicine · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsDefective apoptosis of lamina propria T cells (LPTs) is involved in the pathogenesis of Crohn's disease. Survivin, a member of the inhibitors of apoptosis family, prevents cell death and regulates cell division. Survivin has been studied extensively in cancer, but little is known about its role in Crohn's disease.
methodsLPTs were isolated from mucosal samples of patients with Crohn's disease or ulcerative colitis and healthy individuals (controls). LPTs were activated with interleukin-2 or via CD3, CD2, and CD28 signaling, and cultured at 42°C to induce heat shock. Survivin expression was assessed by immunohistochemistry, confocal microscopy, and immunoblotting; survivin levels were reduced by RNA interference. Cell viability, apoptosis, and proliferation were measured by trypan blue exclusion, annexin-V/7-Aminoactinomycin D staining, and uptake of [3]thymidine, respectively.
resultsLPTs from patients with Crohn's disease had higher levels of survivin than LPTs from patients with ulcerative colitis or controls. RNA knockdown of survivin in LPTs inhibited their proliferation and promoted apoptosis. Levels of survivin were low in LPTs from patients with ulcerative colitis and controls as a result of ubiquitin-mediated proteasome degradation. In LPTs from patients with Crohn's disease, survivin bound to the heat shock protein (HSP)90, and therefore was resistant to proteasome degradation. Incubating LPTs with 17-N-allylamino-17-demethoxygeldanamycin, an inhibitor of HSP90, reduced levels of survivin and induced apoptosis.
conclusionsLevels of survivin are increased in LPTs from patients with Crohn's disease (compared with ulcerative colitis and controls) because survivin interacts with HSP90 and prevents proteasome degradation. This allows LPTs to avoid apoptosis. Strategies to restore apoptosis to these cells might be developed to treat patients with Crohn's disease.
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What OpenQuestion holds
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.