ArticleBiotechnology letters2022
BMSCs improve TNBS-induced colitis in rats by inducing Treg differentiation by expressing PD-L1.
Article in Biotechnology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- Ulcerative colitis: signaling pathways, therapeutic targets and interventional strategies.Signal transduction and targeted therapy · 2026Review
- Mesenchymal Stem Cells Modulate Regulatory T Cells: From Molecular Mechanisms to Disease Therapy.Stem cells international · 2026Review
- Comparison of administration methods in adipose tissue-derived stem cell therapy in rats with colitis: An experimental study.Northern clinics of Istanbul · 2025Article
- Therapeutic and immunomodulatory potentials of mesenchymal stromal/stem cells and immune checkpoints related molecules.Biomarker research · 2024Review
- Utility of four machine learning approaches for identifying ulcerative colitis and Crohn's disease.Heliyon · 2024Article
- Quercetin ameliorates ulcerative colitis by restoring the balance of M2/M1 and repairing the intestinal barrier via downregulating cGAS‒STING pathway.Frontiers in pharmacology · 2024Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
objectivesBone marrow-derived mesenchymal stem cells (BMSCs) show promise in treating inflammatory bowel disease. We tested if BMSCs improve Trinitro-benzene-sulfonic acid (TNBS)-induced colitis by inducing Treg differentiation by modulating programmed cell death 1 ligand 1(PD-L1).
resultsBMSCs were isolated and transfected with PD-L1 siRNA. Sprague-Dawley rats were randomly divided into 4 groups: normal, model, BMSC control, and PD-L1 siRNA BMSC. Colitis was induced by TNBS, except in the normal group. On d4, the BMSC control and PD-L1 siRNA BMSC groups were intravenously injected with BMSCs at a dose of 5 × 10
conclusionsWe found that BMSCs can induce Treg differentiation by inhibiting the Akt/mTOR pathway via PD-L1; this significantly improved symptoms and pathology in our ulcerative colitis rat models.
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Registered trials
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