We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Notch1 signaling induces epithelial-mesenchymal transition in lens epithelium cells during hypoxia.
- Authors
Lei Liu; Wei Xiao; Liu, Lei; Xiao, Wei
- Abstract
<bold>Background: </bold>Posterior Capsular Opacification (PCO) is one of the most common complications of cataract surgery which can result in severe visual damage. Epithelial-Mesenchymal Transition (EMT) of lens epithelium cells (LEC) is the pathological basis of PCO. Recent research showed that hypoxia acted as an inducer of EMT through a Notch1/Snail1/E-cadherin pathway. However, it remains unclear whether the Notch1/Snail1/E-cadherin pathway is involved in PCO under hypoxia.<bold>Methods: </bold>The morphology of SRA01/04 cells treating with Cobalt Chloride (CoCl2) was observed and the markers of EMT and Notch1/Snail1/E-cadherin pathway were analyzed by Western blot and Immunocytochemistry assay. Transwell invasion assay and Wound healing assay were used to detected the effect of p3 × FLAG-CMV-7-NICD1 transfection on the SRA01/04 cells.<bold>Results: </bold>The SRA01/04 cells lost cell polarity and cell junction culturing with CoCl2. The expression of Keratin, Hypoxia-inducible factor-1 alpha (HIF-1α), Notch1, Snail1were upregulated, on the other side, Fibronectin and E-cadherin were downregulated in hypoxia. Furthermore, the overexpression of Notch1 induced the expression of E-cadherin and increased the invasion and migration ability of SRA01/04 cells.<bold>Conclusions: </bold>These results suggest that Notch1/Snail1/E-cadherin pathway facilitates the EMT through HIF-1α in SRA01/04 cells during hypoxia and promotes LEC motility.
- Subjects
CATARACT surgery; OPHTHALMIC surgery complications; HYPOXIA-inducible factor 1; COBALT chloride; IMMUNOCYTOCHEMISTRY; CELL junctions; CATARACT; CELL culture; CELL physiology; CELL receptors; CELL motility; CELLULAR signal transduction; CRYSTALLINE lens; EPITHELIAL cells; GENES; IMMUNOHISTOCHEMISTRY; RNA; WESTERN immunoblotting
- Publication
BMC Ophthalmology, 2017, Vol 17, p1
- ISSN
1471-2415
- Publication type
journal article
- DOI
10.1186/s12886-017-0532-1