Inflammatory cytokine TNF-α promotes corneal endothelium apoptosis via upregulating TIPE2 transcription during corneal graft rejection.

Graefe's Archive for Clinical and Experimental Ophthalmology = Albrecht Von Graefes Archiv Für Klinische Und Experimentelle Ophthalmologie
Qun WangWeiyun Shi

Abstract

Endothelial dysfunction accounts for 50% of total corneal transplantation failures, suggesting that corneal endothelial damage is the leading cause of graft failure. Tumor necrosis factor-α (TNF-α) is known to contribute to the negative regulation of corneal transplantation, but how it does so remains unclear. Here, we report a regulatory loop involving TNF-α, TNF-α-induced protein 8 like 2 (TNFAIP8L2 or TIPE2), and apoptosis during corneal graft rejection. We established mice models of penetrating keratoplasty to verify whether the quantification of TNF-α in allogeneic corneas is enhanced through ELISA assay and immunofluorescence staining. In cornea tissues, we obtained corneal endothelium and measured apoptosis of the removed cells. Meanwhile, quantitative real-time PCR and Western blotting were used to detect the mRNA and protein expression of TIPE2. In human corneal endothelial cells, we verified the conclusions through some experiments. By specifically knocking down TIPE2, we detected the importance of TIPE2 in TNF-α-triggered apoptosis. In mice models, TNF-α was higher in the cornea and aqueous humor in allograft group and TNF-α elevation increased the apoptosis of the corneal endothelium. In addition, high levels of TIP...Continue Reading

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Citations

Aug 5, 2020·Investigative Ophthalmology & Visual Science·Nozomi IgarashiMakoto Aihara
Sep 1, 2019·Stem Cell Research & Therapy·Na LiRuihua Wei

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