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Effects of atorvastatin on the function of Tenon's capsule fibroblasts in human eyes
Haiying Wei1, Jian Wang1, Ruiqi Wang1
1Eye Hospital, The First Affiliated Hospital of Harbin Medical University, Key Laboratory of Basic and Clinical Research of Heilongjiang Province, No. 23, Youzheng Street, Nangang District, Harbin, 150001, Heilongjiang, China.
Purpose:
This study aimed to explore the role of atorvastatin (ATO) in the prevention and treatment of the scarring of filtration channels after glaucoma surgery.
Methods:
Human Tenon's capsule fibroblasts (HTFs) were co-cultured with various concentrations of ATO. First, Cell Counting Kit-8 assay was performed to evaluate the effects of various concentrations of ATO on the viability of HTFs. Then, after the ATO stimulated the HTFs for 24 h, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay was performed to evaluate the apoptosis of HTFs. Transwell assay was also performed to evaluate the migration of HTFs. Moreover, enzyme-linked immunosorbent assay (ELISA) was performed to detect the protein expression levels of transforming growth factor-β1 (TGF-β1) and TGF-β2 in the cell culture supernatant of HTFs. Western blot was carried out to detect the protein expression levels of smooth muscle actin (SMA), p38, Smad3, fibronectin, collagen I and collagen III in different groups.
Results:
The results revealed that ATO could inhibit the proliferation and migration of HTFs. Based on the TUNEL assay, 100 μM and 150 μM ATO could induce cell apoptosis. The ELISA results indicated that ATO could down-regulate the expression level of TGF-β2, and western blot analysis revealed that the protein expression levels of SMA, p38, Smad3, fibronectin, collagen I and collagen III in the TGF-β2 group were all up-regulated compared with the control group, whereas the addition of ATO could reverse this up-regulation.
Conclusions:
ATO could inhibit the proliferation and migration of HTFs and induce their apoptosis. It was preliminary proven that ATO could inhibit the signaling pathway induced by TGF-β. It is suggested that ATO could be a basis for the treatment of the scarring of filtration channels after glaucoma surgery.
Insights
Atorvastatin (ATO) inhibits human Tenon's capsule fibroblast proliferation and migration, inducing apoptosis. This suggests ATO may prevent scarring after glaucoma surgery by modulating TGF-β signaling.
Area of Science:
- Ophthalmology
- Cell Biology
- Pharmacology
Background:
- Glaucoma surgery aims to reduce intraocular pressure.
- Filtration channel scarring is a major cause of surgical failure.
- Identifying agents to prevent scarring is crucial for improving surgical outcomes.
Purpose of the Study:
- To investigate the role of atorvastatin (ATO) in preventing and treating filtration channel scarring post-glaucoma surgery.
- To determine ATO's effects on human Tenon's capsule fibroblasts (HTFs).
Main Methods:
- HTFs were treated with varying ATO concentrations.
- Cell Counting Kit-8, TUNEL, and Transwell assays assessed viability, apoptosis, and migration.
- ELISA and Western blot analyzed TGF-β1, TGF-β2, SMA, p38, Smad3, fibronectin, collagen I, and collagen III expression.
Main Results:
- ATO inhibited HTF proliferation and migration.
- High ATO concentrations (100-150 μM) induced HTF apoptosis.
- ATO downregulated TGF-β2 expression and reversed TGF-β2-induced upregulation of SMA, p38, Smad3, fibronectin, collagen I, and collagen III.
Conclusions:
- ATO demonstrates anti-proliferative, anti-migratory, and pro-apoptotic effects on HTFs.
- ATO appears to inhibit the TGF-β signaling pathway.
- ATO shows potential as a therapeutic agent for preventing filtration channel scarring after glaucoma surgery.
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