Lysosomal chymotrypsin B potentiates apoptosis via cleavage of Bid
Identifieur interne : 001698 ( Main/Exploration ); précédent : 001697; suivant : 001699Lysosomal chymotrypsin B potentiates apoptosis via cleavage of Bid
Auteurs : Kai Zhao [République populaire de Chine] ; Xingyu Zhao [République populaire de Chine] ; Yaping Tu [États-Unis] ; Qi Miao [République populaire de Chine] ; Dongxu Cao [République populaire de Chine] ; Wenjuan Duan [République populaire de Chine] ; Yang Sun [République populaire de Chine] ; Jincheng Wang [République populaire de Chine] ; Taotao Wei [République populaire de Chine] ; Fuyu Yang [République populaire de Chine]Source :
- Cellular and Molecular Life Sciences [ 1420-682X ] ; 2010-08-01.
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Abstract
Abstract: We have reported that chymotrypsin B (CtrB) is not just a digestive enzyme but is also stored in lysosomes. Herein, we demonstrated a broad distribution of CtrB and explored the involvement of CtrB in apoptosis. Exposure of RH-35 cells to H2O2 or palmitate induced the redistribution of lysosomal CtrB into the cytoplasm as a result of lysosomal membrane permeabilization (LMP). Suppression of CtrB significantly blocked apoptosis, while overexpression of CtrB sensitized apoptosis markedly. CtrB could cleave Bid under neutral conditions. In RH-35 cells with Bid silenced, apoptosis induced by CtrB protein was attenuated, suggesting that CtrB mediates apoptosis of RH-35 cells mainly through processing Bid. Our data also suggest that LMP occurs earlier than mitochondrial outer membrane permeabilization; Bid activation initiated by caspase-8 might be reinforced by CtrB in consequence of LMP, which causes a positive feedback loop leading to the accumulation of tBid, and results in lysosome- and mitochondrion-dependent apoptosis.
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DOI: 10.1007/s00018-010-0356-0
Affiliations:
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Mol. Life Sci.</title><idno type="ISSN">1420-682X</idno><idno type="eISSN">1420-9071</idno><imprint><publisher>SP Birkhäuser Verlag Basel</publisher><pubPlace>Basel</pubPlace><date type="published" when="2010-08-01">2010-08-01</date><biblScope unit="volume">67</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2665">2665</biblScope><biblScope unit="page" to="2678">2678</biblScope></imprint><idno type="ISSN">1420-682X</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1420-682X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis</term><term>Bid</term><term>Chymotrypsin B</term><term>Lysosome</term><term>Mitochondrion</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: We have reported that chymotrypsin B (CtrB) is not just a digestive enzyme but is also stored in lysosomes. Herein, we demonstrated a broad distribution of CtrB and explored the involvement of CtrB in apoptosis. Exposure of RH-35 cells to H2O2 or palmitate induced the redistribution of lysosomal CtrB into the cytoplasm as a result of lysosomal membrane permeabilization (LMP). Suppression of CtrB significantly blocked apoptosis, while overexpression of CtrB sensitized apoptosis markedly. CtrB could cleave Bid under neutral conditions. In RH-35 cells with Bid silenced, apoptosis induced by CtrB protein was attenuated, suggesting that CtrB mediates apoptosis of RH-35 cells mainly through processing Bid. Our data also suggest that LMP occurs earlier than mitochondrial outer membrane permeabilization; Bid activation initiated by caspase-8 might be reinforced by CtrB in consequence of LMP, which causes a positive feedback loop leading to the accumulation of tBid, and results in lysosome- and mitochondrion-dependent apoptosis.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li><li>États-Unis</li></country><region><li>Nebraska</li></region><settlement><li>Pékin</li></settlement></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Zhao, Kai" sort="Zhao, Kai" uniqKey="Zhao K" first="Kai" last="Zhao">Kai Zhao</name></noRegion><name sortKey="Cao, Dongxu" sort="Cao, Dongxu" uniqKey="Cao D" first="Dongxu" last="Cao">Dongxu Cao</name><name sortKey="Duan, Wenjuan" sort="Duan, Wenjuan" uniqKey="Duan W" first="Wenjuan" last="Duan">Wenjuan Duan</name><name sortKey="Duan, Wenjuan" sort="Duan, Wenjuan" uniqKey="Duan W" first="Wenjuan" last="Duan">Wenjuan Duan</name><name sortKey="Miao, Qi" sort="Miao, Qi" uniqKey="Miao Q" first="Qi" last="Miao">Qi Miao</name><name sortKey="Sun, Yang" sort="Sun, Yang" uniqKey="Sun Y" first="Yang" last="Sun">Yang Sun</name><name sortKey="Wang, Jincheng" sort="Wang, Jincheng" uniqKey="Wang J" first="Jincheng" last="Wang">Jincheng Wang</name><name sortKey="Wang, Jincheng" sort="Wang, Jincheng" uniqKey="Wang J" first="Jincheng" last="Wang">Jincheng Wang</name><name sortKey="Wei, Taotao" sort="Wei, Taotao" uniqKey="Wei T" first="Taotao" last="Wei">Taotao Wei</name><name sortKey="Wei, Taotao" sort="Wei, Taotao" uniqKey="Wei T" first="Taotao" last="Wei">Taotao Wei</name><name sortKey="Yang, Fuyu" sort="Yang, Fuyu" uniqKey="Yang F" first="Fuyu" last="Yang">Fuyu Yang</name><name sortKey="Yang, Fuyu" sort="Yang, Fuyu" uniqKey="Yang F" first="Fuyu" last="Yang">Fuyu Yang</name><name sortKey="Zhao, Kai" sort="Zhao, Kai" uniqKey="Zhao K" first="Kai" last="Zhao">Kai Zhao</name><name sortKey="Zhao, Xingyu" sort="Zhao, Xingyu" uniqKey="Zhao X" first="Xingyu" last="Zhao">Xingyu Zhao</name><name sortKey="Zhao, Xingyu" sort="Zhao, Xingyu" uniqKey="Zhao X" first="Xingyu" last="Zhao">Xingyu Zhao</name></country><country name="États-Unis"><region name="Nebraska"><name sortKey="Tu, Yaping" sort="Tu, Yaping" uniqKey="Tu Y" first="Yaping" last="Tu">Yaping Tu</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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