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• W2135204562 abstract "Abstract Background and Aim: It is well known that tumor necrosis factor‐α (TNF‐α) induces hepatocyte apoptosis and contributes to liver diseases. However, the exact mechanisms are not well understood. Methods: In the present study, we reported that Na + /H + exchanger (NHE) is involved in TNF‐α‐induced hepatocyte apoptosis. Results: TNF‐α time dependently induced an increase in NHE activity in hepatocytes, but cariporide, an NHE inhibitor, blocked the TNF‐α‐induced increase of NHE activity in a dose‐dependent manner. Increased NHE activity induced by TNF‐α was associated with increased intracellular calcium (Ca 2+ i ) concentration and calpain activity. Cariporide reversed these effects induced by TNF‐α. In addition, TNF‐α downregulated Bcl‐xL, an anti‐apoptotic protein, but not mRNA levels. The inhibition of either calpain or NHE blocked the TNF‐α‐induced decrease of the Bcl‐xL protein. TNF‐α did not change the pro‐apoptotic Bax and Bak protein levels. Cariporide, calcium remover 1,2‐bis (2‐aminophenoxy) ethane‐N,N,N0,N0–tetraacetic acid, or calpain inhibitor benzyloxycarbonyl‐leucyl‐leucinal attenuated TNF‐α‐induced hepatocyte apoptosis. Conclusion: TNF‐α via NHE results in hepatocyte apoptosis through the calcium/calpain/Bcl‐xL pathway." @default.
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• W2135204562 date "2009-05-01" @default.
• W2135204562 modified "2023-10-16" @default.
• W2135204562 title "Na⁺/H⁺exchanger mediates TNF-α-induced hepatocyte apoptosis via the calpain-dependent degradation of Bcl-xL" @default.
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• W2135204562 doi "https://doi.org/10.1111/j.1440-1746.2008.05715.x" @default.
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