Experimental eye research · 2026
PSAT1 regulates the proliferation, migration, and EMT of oxidatively damaged lens epithelial cells through activation of the JNK/c-Jun pathway.
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Yang Qing, Fu Lingzhi, Sun Feng, Han Yuanyuan, Chen Yaru, Xu Mengyue, Liu Yan, Wang Jianfeng
Аннотация
OBJECTIVE: This study aims to explore the impacts and the fundamental mechanisms underlying the influence of Phosphoserine Aminotransferase 1 (PSAT1) on the proliferative capabilities, migratory tendencies, and the epithelial-mesenchymal transition (EMT) exhibited by human lens epithelial cells within an environment of oxidative stress.
METHODS: Anterior capsular membrane tissues were collected from patients with ocular trauma and ARC requiring surgery. Oxidative stress models were established in vitro using H2O2 in both rat cataract models and HLEC cell lines. siRNA and overexpression plasmids were used to modulate PSAT1 activity. To determine the expression profiles of genes and proteins, we employed immunofluorescence Staining, immunohistochemical staining methodologies, alongside qRT-PCR and WB assessments.
RESULTS: PSAT1 was highly expressed in the anterior capsular membrane of ARC lenses, the lenses of rat cataract models, and oxidatively stressed HLECs. H2O2 treatment enhanced HLEC migration, and EMT, and suppressed cell proliferation, while activating the JNK/c-Jun signaling pathway. PSAT1 interference reversed these effects. Overexpression of PSAT1 in oxidatively stressed HLECs further promoted cell migration, EMT, and JNK/c-Jun signaling, suppressing cell proliferation. Inhibition of the JNK pathway reversed these outcomes.
CONCLUSION: PSAT1 may promote migration, and EMT, and suppress proliferation in oxidatively stressed HLECs by activating the JNK/c-Jun signaling pathway.
METHODS: Anterior capsular membrane tissues were collected from patients with ocular trauma and ARC requiring surgery. Oxidative stress models were established in vitro using H2O2 in both rat cataract models and HLEC cell lines. siRNA and overexpression plasmids were used to modulate PSAT1 activity. To determine the expression profiles of genes and proteins, we employed immunofluorescence Staining, immunohistochemical staining methodologies, alongside qRT-PCR and WB assessments.
RESULTS: PSAT1 was highly expressed in the anterior capsular membrane of ARC lenses, the lenses of rat cataract models, and oxidatively stressed HLECs. H2O2 treatment enhanced HLEC migration, and EMT, and suppressed cell proliferation, while activating the JNK/c-Jun signaling pathway. PSAT1 interference reversed these effects. Overexpression of PSAT1 in oxidatively stressed HLECs further promoted cell migration, EMT, and JNK/c-Jun signaling, suppressing cell proliferation. Inhibition of the JNK pathway reversed these outcomes.
CONCLUSION: PSAT1 may promote migration, and EMT, and suppress proliferation in oxidatively stressed HLECs by activating the JNK/c-Jun signaling pathway.