AI Article Synopsis
- The study investigates how tacrolimus affects TGFβ signaling in intestinal epithelial cells (IECs) during colitis induced by dextran sulfate sodium (DSS).
- Results show that tacrolimus reduces IEC apoptosis and mucosal damage even when TGFβ is inhibited.
- The drug enhances the expression of key signaling proteins (like TGFβ-RII and phosphor-SMAD) through the ERK pathway, offering protection against intestinal epithelial injury.
Article Abstract
Background/aim: Transforming growth factor β (TGFβ) signaling plays a key role in modulating intestinal epithelial cell (IEC) homeostasis. The present study aimed to investigate the direct effect of tacrolimus on TGFβ signaling in IECs.
Materials And Methods: The protective effects of tacrolimus, with or without anti-TGFβ antibody, in dextran sulfate sodium (DSS)-induced colitis were evaluated.
Results: Tacrolimus ameliorated IEC apoptosis-mediated mucosal destruction despite anti-TGFβ treatment. TGFβ receptor type II (TGFβ-RII), phosphor-SMAD family members 2/3, and phosphor-extracellular signal-regulated kinase (ERK) expression in IECs was enhanced in tacrolimus-treated mice, and these positive effects were maintained despite anti-TGFβ treatment. Moreover, tacrolimus induced TGFβ-RII up-regulation through ERK activation.
Conclusion: Our data indicate that tacrolimus directly activated TGFβ-SMAD signaling via the ERK pathway in IECs, thereby providing protection against apoptosis-mediated intestinal epithelial injury.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9301428 | PMC |
| http://dx.doi.org/10.21873/invivo.12880 | DOI Listing |
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