Transforming growth factorβ (TGFβ) is important in the development of posterior capsule opacification (PCO), and inhibition of the TGFβ pathway may represent a novel method of treating PCO. Drosophila protein, mothers against decapentaplegic homolog 3 (Smad3) is
a phosphorylated receptoractivated Smad required for the transmission of TGFβ signals. Smad3 knockout (KO) disturbs the activation of TGFβ 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 26gauge hypodermic needle. The effect of Smad3 in the traumainduced epithelialmesenchymal transition (EMT) of the lens epithelium in Smad3KO and wildtype (WT) mice was then observed. The expression levels of EMT markers and extracellular
matrix components were measured in the two groups by reverse transcriptionquantitative polymerase chain reaction analysis, western blot analysis and immunofluorescence staining. Apoptosis was also detected in the punctured anterior capsule. The Smad3KO mice exhibited lower expression levels
of αsmooth muscle actin, lumican, osteopontin, fibronectin and collagen, compared with the WT mice. Additionally, the Smad3KO mice exhibited a higher percentage of apoptotic cells than the WT mice. Smad3 signaling was associated with the induction of traumainduced EMT, and Smad3 KO interfered
with TGFβ signaling pathway activation, but did not completely inhibit the traumainduced EMT in LECs. Therefore, Smad3 may be a target in the treatment of PCO and other fibrosisrelated diseases.
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Document Type: Research Article
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
Publication date: January 1, 2018
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The International Journal of Molecular Medicine is a monthly, peer-reviewed journal devoted to the publication of high quality studies related to the molecular mechanisms of human disease. The journal welcomes research on all aspects of molecular and clinical research, ranging from biochemistry to immunology, pathology, genetics, human genomics, microbiology, molecular pathogenesis, molecular cardiology, molecular surgery and molecular psychology.
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