Transfection of hepatic stimulator substance gene desensitizes hepatoma cells to H2O2-induced cell apoptosis via preservation of mitochondria.
نویسندگان
چکیده
Hepatic stimulator substance (HSS) protects liver cells from various toxins. However, the mechanism by which HSS protects hepatocytes remains unclear. In this study, we report that the HSS gene, after transfection into BEL-7402 hepatocma cells, is stably expressed in the mitochondria. Hydrogen peroxide (H(2)O(2))-induced cell apoptosis in the HSS-transfected cells is reduced, as shown by morphologic analysis. In the HSS-transfected cells, disruption of mitochondrial transmembrane potential (MTP) and cytochrome c leakage are reduced. The anti-apoptotic gene Bcl-2 is also highly expressed. In addition, ATP levels in the HSS-transfected cells are maintained. In conclusion, in hepatoma cells, HSS gene expression protects cells against H(2)O(2) injury, and this effect is likely to be associated with preservation of mitochondria.
منابع مشابه
The conserved CXXC motif of hepatic stimulator substance is essential for its role in mitochondrial protection in H2O2-induced cell apoptosis.
Hepatic stimulator substance (HSS) protects liver cells from various toxins by alleviating lesions caused in the mitochondria. This paper demonstrates the necessity of the conserved CXXC catalytic motif (C62-C65) for the mitochondria-targeted anti-apoptotic activity of HSS. Mutating the conserved CXXC motif eliminated the protective effects against H(2)O(2)-induced apoptosis and diminished the ...
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ورودعنوان ژورنال:
- Archives of biochemistry and biophysics
دوره 464 1 شماره
صفحات -
تاریخ انتشار 2007