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Quantification of the Immunosuppressant Tacrolimus on Dried Blood Spots Using LC-MS/MS

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Published on: November 8, 2015

Tacrolimus Inhibits Human Tenon's Fibroblast Migration, Proliferation, and Transdifferentiation.

Woojune Hur^1,2, Jeongeun Park², Jae-Hyuck Lee¹

¹Department of Ophthalmology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Republic of Korea.

|December 30, 2025

Summary

This summary is machine-generated.

Tacrolimus inhibits human Tenon

Keywords:

Smad-dependent pathway human Tenon’s fibroblast tacrolimus

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Last Updated: Jan 7, 2026

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Area of Science:

Ophthalmology
Cell Biology
Immunology

Background:

Human Tenon's fibroblasts (HTFs) play a crucial role in ocular wound healing and fibrosis.
Understanding factors that modulate HTF behavior is essential for developing anti-fibrotic therapies in ophthalmology.

Purpose of the Study:

To investigate the in vitro effects of tacrolimus on human Tenon's fibroblast (HTF) migration, proliferation, and transdifferentiation.
To elucidate the signaling pathways involved in tacrolimus's action on HTFs.

Main Methods:

HTF cells were treated with tacrolimus, platelet-derived growth factor (PDGF), or transforming growth factor beta-1 (TGF-β1).
Cell migration and proliferation were assessed using scratch assays and WST-1 assays, respectively.
Western blotting was used to analyze protein expression, including phosphorylated Smad2, Smad3, ERK, and Akt, to investigate TGF-β signaling pathway involvement.

Main Results:

PDGF and TGF-β1 significantly enhanced HTF migration, proliferation, and transdifferentiation.
Tacrolimus inhibited these pro-fibrotic effects induced by both PDGF and TGF-β1.
Tacrolimus suppressed the TGF-β1-induced phosphorylation of Smad2 and Smad3, indicating inhibition of the TGF-β signaling pathway.

Conclusions:

Tacrolimus effectively inhibits PDGF- and TGF-β1-induced HTF migration, proliferation, and transdifferentiation.
The inhibitory mechanism of tacrolimus involves the Smad-dependent TGF-β signaling pathway.
Further in vivo and clinical studies are warranted to explore tacrolimus as a potential therapeutic agent for ocular fibrotic conditions.