期刊
EXPERIMENTAL EYE RESEARCH
卷 181, 期 -, 页码 145-149出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exer.2019.01.016
关键词
Lens epithelial cell; ROCK inhibitor; Epithelial-to-mesenchymal transition; Transforming growth factor-beta; Type I collagen
资金
- Japan Society for the Promotion of Science KAKENHI [17K11465]
- Grants-in-Aid for Scientific Research [17K11465] Funding Source: KAKEN
The deposition of extracellular matrix (ECM)-which is mainly composed of type I collagen-in anterior subcapsular cataracts (ASCs) during epithelial-to-mesenchymal transition (EMT) of lens epithelial cells (LECs) decreases visual function. Transforming growth factor (TGF)-beta is a key factor in the induction of EMT in LECs. Although Rho kinase (ROCK) plays an important role in EMT induced by TGF-5, it is unknown whether ROCK inhibition affects type I collagen expression in TGF-beta-stimulated LECs and ASC formation. This was investigated in the present study both in vitro using human lens epithelium (HLE)-B3 cells and in vivo using mice with ultraviolet radiation (UVR)-B-induced cataracts. We found that TGF-beta 2 increased type I collagen mRNA expression in HLE-B3 cells; this was inhibited in a dose-dependent manner by treatment with the ROCK inhibitor Y27632. UVR-B exposure caused ASC formation in mice. A histopathological examination revealed that LECs in the anterior subcapsular area were flattened and multi-layered, and had a spindle shape in cross section. Immunohistochemical analysis revealed the presence of a-smooth muscle actin and type I collagen around these flattened LECs; these opacities were reduced by topical instillation of Y-27632. These findings suggest that suppression of TGF-beta signaling in LECs by topical application of a ROCK inhibitor can prevent the formation of ASCs.
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