Knockdown of FAM225B inhibits the progression of the hypertrophic scar following glaucoma surgery by inhibiting autophagy
Affiliations: Department of Dermatology, Affiliated Hospital of Beihua University, Jilin, Jilin 132001, P.R. China
- Published online on: January 14, 2021 https://doi.org/10.3892/mmr.2021.11843
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The formation of a hypertrophic scar (HS) may lead to failure of glaucoma surgery. Long non‑coding RNAs (lncRNAs) are involved in the formation of HSs. Moreover, family with sequence similarity 225 member B (FAM225B) is upregulated in HS. However, the role of the lncRNA FAM225B in HS remains unknown. Thus, the present study aimed to investigate the function of FAM225B in HS. Scar fibroblasts were isolated from patients who had undergone glaucoma surgery. Western blotting was used to detect the expressions of Bax, Bcl‑2, cleaved caspase 3, p62, ATG7 and Beclin 1, and reverse transcription‑quantitative PCR (RT‑qPCR) were conducted to determine the level of FAM225B in scar fibroblasts. Microtubule associated protein 1 light chain 3 α staining was performed to examine autophagosomes in scar fibroblasts. Furthermore, cell proliferation was evaluated via 5‑ethynyl‑2'‑deoxyuridine staining. Flow cytometry was conducted to determine cell apoptosis and the levels of reactive oxygen species (ROS) in scar fibroblasts. The cell migratory ability was assessed using a Transwell assay. The results demonstrated that FAM225B knockdown significantly attenuated scar fibroblast proliferation and induced apoptosis. Additionally, transfection of scar fibroblasts with FAM225B small interfering RNA (siRNA) significantly increased the ROS levels and significantly decreased the migration of scar fibroblasts. The FAM225B overexpression‑induced increase of scar fibroblast proliferation and migration was significantly reversed by 3‑methyladenine administration. The results suggested that knockdown of FAM225B significantly inhibited the proliferation of scar fibroblasts by inhibiting autophagy. Therefore, knockdown of FAM225B could inhibit scar fibroblast proliferation after glaucoma surgery by inhibiting autophagy. These findings may provide a novel perspective of developing treatment strategy for the patients with HSs after glaucoma surgery.