期刊
JOURNAL OF CELL SCIENCE
卷 131, 期 22, 页码 -出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.217240
关键词
Lens; TGF beta; Epithelial-mesenchymal transition; Fibrosis; Cataract
类别
资金
- National Eye Institute of the National Institutes of Health [R01EY022113, R01EY028558]
- Medical Research Foundation of Oregon [1611]
- NATIONAL EYE INSTITUTE [R01EY028558, R01EY022113] Funding Source: NIH RePORTER
Lens epithelial cells are bound to the lens extracellular matrix capsule, of which laminin is a major component. After cataract surgery, surviving lens epithelial cells are exposed to increased levels of fibronectin, and so we addressed whether fibronectin influences lens cell fate, using DCDML cells as a serum-free primary lens epithelial cell culture system. We found that culturing DCDMLs with plasma-derived fibronectin upregulated canonical TGF beta signaling relative to cells plated on laminin. Fibronectin-exposed cultures also showed increased TGF beta signaling-dependent differentiation into the two cell types responsible for posterior capsule opacification after cataract surgery, namely myofibroblasts and lens fiber cells. Increased TGF beta activity could be identified in the conditioned medium recovered from cells grown on fibronectin. Other experiments showed that plating DCDMLs on fibronectin overcomes the need for BMP in fibroblast growth factor (FGF)-induced lens fiber cell differentiation, a requirement that is restored when endogenous TGF beta signaling is inhibited. These results demonstrate how the TGF beta-fibronectin axis can profoundly affect lens cell fate. This axis represents a novel target for prevention of late-onset posterior capsule opacification, a common but currently intractable complication of cataract surgery.
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