Abstract：
:Tau truncation is widely detected in Alzheimer's disease brain. Caspases activation is suggested to play a significant role in tau truncation at Aspartate 421 (D421) according to their ability to cleave recombinant tau in vitro. Ample evidence has shown that caspase-6 is involved in cognitive impairment and expressed in AD brain. Reactive oxygen species (ROS) can lead to caspase-6 activation and correlate with AD. Here, we transfected human embryonic kidney 293 (HEK 293) cells with Tau 441 plasmid and investigated the role of caspase-6 and caspase-3 in ROS-mediated tau truncation. Our data demonstrated that H2O2 induced oxidative stress and increased tau truncation. Caspase-6 and caspase-3 activity also increased in a dose-dependent manner in HEK 293/Tau cells during H2O2 insult. When cells were treated with an ROS inhibitor N-acetyl-L-cysteine, tau truncation was significantly suppressed. Compared with H2O2 (100 μM)/non-inhibitor group or single-inhibitor groups (z-VEID-fmk, caspase-6 inhibitor or z-DEVD-fmk, and caspase-3 inhibitor), tau truncation induced by H2O2 was effectively reduced in the combinative inhibitors group. Similar results were shown when cells were transfected with specific caspase-3 and caspase-6 siRNA. Inhibition of caspase-6 led to decline of caspase-3 activation. Taken together, our results suggest that the combination of caspase-6 and caspase-3 aggravates tau truncation at D421 induced by H2O2. Caspase-6 may play an important part in activating caspase-3. Further investigation of how the synergic role of caspase-6 and caspase-3 affects tau truncation may provide new visions for potential AD therapies.
journal_name
Cell Mol Neurobioljournal_title
Cellular and molecular neurobiologyauthors
Zhao H,Zhao W,Lok K,Wang Z,Yin Mdoi
10.1007/s10571-013-0021-xsubject
Has Abstractpub_date
2014-04-01 00:00:00pages
369-78issue
3eissn
0272-4340issn
1573-6830journal_volume
34pub_type
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