Role of Smad3 signaling in the epithelial‑mesenchymal transition of the lens epithelium following injury

Meng,Fanlan; Li,Jun; Yang,Xiao; Yuan,Xiaoyong; Tang,Xin

doi:10.3892/ijmm.2018.3662

Role of Smad3 signaling in the epithelial‑mesenchymal transition of the lens epithelium following injury

Authors:
- Fanlan Meng
- Jun Li
- Xiao Yang
- Xiaoyong Yuan
- Xin Tang
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Affiliations: Clinical College of Ophthalmology, Tianjin Medical University, Tianjin 300020, P.R. China, The State Key Laboratory of Proteomics, Genetics Laboratory of Development and Disease, Institute of Biotechnology, AMMS, Beijing 100071, P.R. China
Published online on: May 9, 2018 https://doi.org/10.3892/ijmm.2018.3662
Pages: 851-860
Copyright: © Meng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Transforming growth factor‑β (TGF‑β) is important in the development of posterior capsule opacification (PCO), and inhibition of the TGF‑β pathway may represent a novel method of treating PCO. Drosophila protein, mothers against decapentaplegic homolog 3 (Smad3) is a phosphorylated receptor‑activated Smad required for the transmission of TGF‑β signals. Smad3 knockout (KO) disturbs the activation of TGF‑β signaling, thus inhibiting the onset of PCO. In the present study, lens epithelial cell (LEC) damage induced by extracapsular cataract extraction was simulated by puncture of the anterior capsule using a 26‑gauge hypodermic needle. The effect of Smad3 in the trauma‑induced epithelial‑mesenchymal transition (EMT) of the lens epithelium in Smad3‑KO and wild‑type (WT) mice was then observed. The expression levels of EMT markers and extracellular matrix components were measured in the two groups by reverse transcription‑quantitative polymerase chain reaction analysis, western blot analysis and immunofluorescence staining. Apoptosis was also detected in the punctured anterior capsule. The Smad3‑KO mice exhibited lower expression levels of α‑smooth muscle actin, lumican, osteopontin, fibronectin and collagen, compared with the WT mice. Additionally, the Smad3‑KO mice exhibited a higher percentage of apoptotic cells than the WT mice. Smad3 signaling was associated with the induction of trauma‑induced EMT, and Smad3 KO interfered with TGF‑β signaling pathway activation, but did not completely inhibit the trauma‑induced EMT in LECs. Therefore, Smad3 may be a target in the treatment of PCO and other fibrosis‑related diseases.

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