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Updated: Feb 25, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
Published on: February 28, 2017
Notch1 signaling induces epithelial-mesenchymal transition in lens epithelium cells during hypoxia
1Department of Ophthalmology, Shengjing Hospital, China Medical University, NO.36 Sanhao Street, Shenyang City, Liaoning Province, 110004, China.
Background:
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.
Methods:
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.
Results:
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.
Conclusions:
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.
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