MSC secretes certain factors that accelerate corneal re-epithelialisation. The paracrine effects of MSC on corneal wound healing including improvements in cell viability, migration and ECM formation.

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L-carnitine (Lc) is well known for its antioxidative properties. The present study aimed to evaluate the effects of Lc on human lens epithelial cells (HLEcs) and to analyze its regulatory mechanism in cataractogenesis. HLE B-3 cells were cultured with hydrogen peroxide (H 2 O 2 ) and were pretreated with or without Lc. The cell counting kit-8 assay was used to determine cell viability. Reactive oxygen species (ROS) assay kit was used to measure the cellular ROS production induced by H 2 O 2 and Lc. In addition, reverse transcription-quantitative PcR and western blot analysis were performed to detect the expression levels of oxidative damage markers and antioxidant enzymes. Notably, ROS overproduction was observed upon exposure to H 2 O 2 , whereas Lc supplementation markedly decreased ROS levels through activation of the antioxidant enzymes forkhead box O1, peroxiredoxin 4 and catalase. Furthermore, Lc suppressed the expression of apoptosis-associated genes (caspase-3) and inflammation-associated genes [interleukin (IL)1, IL6, IL8 and cyclooxygenase-2]. conversely, Lc promoted proliferating cell nuclear antigen, cyclin-dependent kinase (cdK)2 and cdK4 expression, which may increase proliferation of HLEcs that were incubated with H 2 O 2 . In addition, epithelial-mesenchymal transition occurred upon ROS accumulation, whereas the effects of H 2 O 2 on AQP1 and vimentin expression were reversed upon Lc supplementation. Notably, this study revealed that Lc restored the oxidant/antioxidant balance and protected against cell damage through the mitogen-activated protein kinase signaling pathway. In conclusion, Lc may serve a protective role in curbing oxidative damage and therefore may be considered a potential therapeutic agent for the treatment of cataracts.

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.