Role of Chondroitin Sulfate Proteoglycan 5 in Steroid-Induced Cataract
Woong-Sun Yoo,
Hyemin Seong,
Chieun Song,
Mee-Young Choi,
Bina Lee,
Youngsub Eom,
Hae-Jin Kim,
Seung Pil Yun,
Seong-Jae Kim
Affiliations
Woong-Sun Yoo
Department of Ophthalmology, Gyeongsang National University College of Medicine, and Gyeongsang National University Hospital, Jinju 52727, Republic of Korea
Hyemin Seong
Department of Ophthalmology, Gyeongsang National University College of Medicine, and Gyeongsang National University Hospital, Jinju 52727, Republic of Korea
Chieun Song
Department of Ophthalmology, Gyeongsang National University College of Medicine, and Gyeongsang National University Hospital, Jinju 52727, Republic of Korea
Mee-Young Choi
Department of Ophthalmology, Gyeongsang National University College of Medicine, and Gyeongsang National University Hospital, Jinju 52727, Republic of Korea
Bina Lee
Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Republic of Korea
Youngsub Eom
Department of Ophthalmology, Korea University College of Medicine, Seoul 02842, Republic of Korea
Hae-Jin Kim
School of Mechanical and Aerospace Engineering, Gyeongsang National University, Jinju 52828, Republic of Korea
Seung Pil Yun
Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Republic of Korea
Seong-Jae Kim
Department of Ophthalmology, Gyeongsang National University College of Medicine, and Gyeongsang National University Hospital, Jinju 52727, Republic of Korea
Steroid-induced cataracts (SIC) are defined as cataracts associated with the administration of corticosteroids. Long-term glucocorticoid treatment for inflammatory diseases reportedly increases the risk of SIC, and steroids can induce cataracts by disrupting ocular growth factor balance or homeostasis. In this study, we verified the effect of chondroitin sulfate proteoglycan 5 (CSPG5) using dexamethasone (dexa)-treated human lens epithelial (HLE-B3) cells and the lens epithelium from the anterior capsule of SIC patients obtained during cataract surgery. CSPG5 expression increased in the lens epithelium of SIC patients. The downregulation of CSPG5 suppressed the dexa-induced epithelial–mesenchymal transition (EMT)-related protein expression and motility in HLE-B3 cells. The disruption of the transcription factors EZH2 and B-Myb downregulated CSPG5, dexa-induced fibronectin expression, and cell migration in HLE-B3 cells, reaffirming that CSPG5 expression regulates EMT in lens epithelial cells. Taken together, these results indicate that the steroid-induced effects on lens epithelial cells are mediated via alterations in CSPG5 expression. Therefore, our study emphasizes the potential of CSPG5 as a therapeutic target for the prevention and treatment of SIC.