Ghrelin Protects Human Lens Epithelial Cells against Oxidative Stress‐Induced Damage

Bai, Jie; Yang, Fan; Liu, Dong; Zheng, Yongri

doi:10.1155/2017/1910450

Cited by 38 publications

(32 citation statements)

References 29 publications

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“…These results were also validated in the lens anterior capsules of cataract patients compared with normal lens anterior capsule samples. Although the increased levels of caspase-1 may indicate the involvement of pyroptosis in the process, it is difficult to distinguish between apoptosis and pyroptosis as apoptosis has also been reported to be involved in cataract formation in H 2 O 2 -treated lens epithelial cells (29). Therefore, further studies are required to address this issue.…”

Section: Discussionmentioning

confidence: 99%

Pyroptosis, a novel mechanism implicated in cataracts

et al. 2018

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An understanding of the mechanism of cataract formation may reduce its burden on medical care worldwide. It is established that pyroptosis is associated with oxidative stress, one of the causes of cataracts, and may provide novel therapeutic targets for the treatment of cataracts. The present study therefore investigated the role of pyroptosis in cataract formation. SRA01/04 human lens epithelium cells (HLECs) were treated with H2O2 and cell viability was assessed by an MTT assay. Pyroptosis in HLECs was examined by TUNEL staining, and the expression of caspase‑1 and interleukin (IL)‑1β was determined using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), western blot analysis and immunostaining. A caspase‑1 inhibitor was used to investigate the effects of caspase‑1 downregulation. In addition, the expression of caspase‑1 and IL‑1β in lens anterior capsule tissue samples from patients with cataracts and normal controls was also analyzed by immunostaining, RT‑qPCR and western blot analysis. The results demonstrated that pyroptosis in H2O2‑treated HLECs, and the mRNA and protein expression of caspase‑1 and IL‑1β, was significantly increased compared with control cells. Furthermore, caspase‑1 and IL‑1β expression was significantly increased in cataract tissue samples compared with normal controls. When HLECs were cotreated with a caspase‑1 inhibitor and 100 µM H2O2, caspase‑1 and IL‑1β expression were decreased compared with the 100 µM H2O2‑only group. In conclusion, the results of the present study demonstrate that pyroptosis may have a role in cataract formation, and the caspase‑1 and IL‑1β pathways may be involved in this pathological process. Pyroptosis appears to be a promising target in the prevention of cataract formation.

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Section: Discussionmentioning

confidence: 99%

Pyroptosis, a novel mechanism implicated in cataracts

et al. 2018

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“…Although the increased expression of caspase-1 and GSDMD and the inhibitory activity of caspase-1 indicate that pyroptosis may be involved in the cataract formation under SWBL exposure, pyroptosis and apoptosis are still di cult to distinguish. It has been reported that apoptosis is involved in cataract formation 18 . Multiple studies show that the characteristic morphological changes of various types of cell death are cell rounding and shrinkage in apoptosis, intact cell membrane and vacuolated cytoplasm in autophagy, and the appearance of membrane bubbles or swelling in pyroptosis [36,37].…”

Section: Discussionmentioning

confidence: 99%

“…Pyroptosis and apoptosis depend on particular caspases to motivate their separate programmed cell death pathways. Pyroptosis can be caused by both canonical and noncanonical in ammasome signalling pathways [15][16][17][18][19][20][21]. Caspase-1, which leads to the cleavage of GSDMD and induces pore opening on the cytomembrane [22][23][24], can activate canonical in ammasome signalling pathway.…”

Section: Introductionmentioning

confidence: 99%

Short-Wavelength Blue Light Contributes to Pyroptosis of Human Lens Epithelial Cells (hLECs) by Caspase-1-GSDMD Signalling Axis Activation

Song¹,

Wang²,

Li³

et al. 2020

Preprint

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Backgroud: To examine the effects of short-wavelength blue light (SWBL) on cultured human lens epithelial cells (hLECs). The nosogenesis of cataracts after SWBL exposure was discussed. Methods: HLE-B3 hLECs were divided into 3 groups randomly: A: normal control group, which consisted of hLECs cultured in the dark; B: the caspase-1 inhibitor group; and C: the SWBL exposure group. After the SWBL (2500 lux) irradiation (for 8, 16, 24, and 32 h), the caspase-1 and gasdermin D (GSDMD) expression levels in HLE-B3 hLECs were examined using ELISA, immunofluorescence, and Western blotting analyses. Double-positive staining of HLE-B3 hLECs for activated and inhibited caspase-1 was used to confirm pyroptosis in hLECs by flow cytometry. Results: SWBL can cause cell death in HLE-B3 hLECs, but a caspase-1 inhibitor suppressed cell death. The flow cytometry results also confirmed the does-dependent of short-wavelength blue light irradiation on pyroptotic death of hLECs. Caspase-1 and GSDMD expression levels of all hLECs groups changed with short-wavelength blue light exposure times (8, 16, 24, and 32 h) and were higher in groups B and C than group A. The immunofluorescence results demonstrated that the expression of GSDMD-N was higher in the cell membrane in both the B and C groups than in the A group.Conclusion: The data indicate that SWBL induces pyroptotic programmed cell death by activation of the GSDMD signalling axis in HLE-B3 hLECs. These results provide new insights into the exploitation of new candidates for the prevention of cataracts.

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“…It is not determined whether this inflammatory protection is due to an increase in both AG and DAG via increased GHRL expression, or whether is the result of a shift in DAG or AG concentrations. Previous studies have linked AG with a plausible role in protecting human lens epithelial cells [36] and osteoblastic cells [37] against reactive oxygen species accumulation. In addition to AG, DAG treatment has also established a protective role from oxidative stress in microvascular endothelial cells via regulation of sirtuin 1 (SIRT1) catalytic activity [38] and within osteoblastic cells independent of GHSR1α [37].…”

Section: Discussionmentioning

confidence: 99%