JOURNAL ARTICLE

Protection of leukemia inhibitory factor against high-glucose-induced human retinal endothelial cell dysfunction

Lei Wang, Qiong Wu, Rui Qi Wang, Run Ze Wang, Jianwen Wang
Archives of Physiology and Biochemistry 2020 July 13, : 1-8
32658632

PURPOSE: In the study, we aimed to explore the mechanism of leukaemia inhibitory factor (LIF) affects hyperglycaemic induced retinopathy by regulating CaMKII-CREB pathway.

METHODS: Human retinal endothelial cell (HRECs) induced by high glucose to simulate one of the pathogenesis in the diabetic retinopathy (DR) model. After LIF treatment, cell viability was detected by CCK-8 and apoptosis was detected by flow cytometry. Angiogenesis was detected by in vitro tube formation. The expression levels of inflammatory, angiogenesis related proteins and CaMKII-CREB were detected by western blot. The gene level of angiogenesis was detected by qRT-PCR. HE staining was used to detect pathological changes of retinopathy in diabetic mice after LIF treatment.

RESULTS: Our results showed that LIF significantly increased hyperglycaemic-induced cell viability and inhibited apoptosis. Western blot results showed that LIF could down-regulate the expression levels of inflammatory cytokines such as IL-1β, IL-6 and TNF-α. In addition, angiogenesis of HRECs was inhibited by LIF in tubulisation experiments. LIF can down-regulate protein and gene levels of VEGF and HIF-1α via western blot and qRT-PCR. In diabetic mice induced by STZ, LIF could down-regulate the protein level of VEGF, HIF-1α, p-CaMKII and p-CREB, which suggest that LIF could inhibit retinal angiogenesis in diabetic mice. The results of HE staining showed that LIF could alleviate the damage of retinopathy in diabetic mice.

CONCLUSION: LIF could alleviate the damage of diabetic retinopathy by modulating the CaMKII/CREB signalling pathway to inhibit inflammatory response and angiogenesis.

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