{'fraction_non_alphanumeric': 0.01949317738791423, 'fraction_numerical': 0.015594541910331383, 'mean_word_length': 5.416666666666667, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Protective roles of Sep15 against cataract formation

Sep15, a 15 KDa selenoprotein, is believed to involve in reduction or isomerization of disulfide bonds and the quality control of glycoprotein folding. However, most of its function remains unclear, especially its roles in the related diseases. For instance, it was reported that Sep15 knockout (KO) mice developed a prominent nuclear cataract in the early of age, but the protective role of Sep15 against cataract formation remains unaddressed. Here, we are trying to share our recent work aimed to unveil the underling mechanism of Sep15 deficiency in cataract development. In our recently published work, we showed that knockdown of Sep15 gene increased human lens epithelial cells’ susceptibility to Tm‐induced stress, and the protective role of Sep15 in human lens epithelial cells was operated via inhibiting oxidative stress. It suggests an interesting perspective to the relevance of Sep15 and cataract formation, i.e. regulating oxidative stress. To follow up, we investigated the effect of Sep15 gene knockdown on differentiation of human lens epithelial cells, since the differentiation of lens epithelial cells to fiber cells is critical to lens transparency. The results showed that Tm‐induced oxidative stress suppressed the expression of β‐crystallin as a lens fiber structural protein, and reduction of Sep15 expression exhibited the similar effect. These results suggested that Sep15 might exert roles on lens fiber cell differentiation by regulating oxidative stress.