Complete activation of autophagic process attenuates liver injury and improves survival in septic mice.
Identifieur interne : 001028 ( Main/Exploration ); précédent : 001027; suivant : 001029Complete activation of autophagic process attenuates liver injury and improves survival in septic mice.
Auteurs : Chih-Wen Lin [Taïwan] ; Steven Lo ; Daw-Shyong Perng ; David Bin-Chia Wu ; Po-Huang Lee ; Ya-Fang Chang ; Po-Lin Kuo ; Ming-Lung Yu ; Shyng-Shiou F. Yuan ; Ya-Ching HsiehSource :
- Shock (Augusta, Ga.) [ 1540-0514 ] ; 2014.
Descripteurs français
- KwdFr :
- Adénine (analogues et dérivés), Adénine (pharmacologie), Animaux, Antiamibiens (pharmacologie), Anticonvulsivants (pharmacologie), Autophagie, Carbamazépine (pharmacologie), Chloroquine (pharmacologie), Foie (anatomopathologie), Foie (métabolisme), Foie (traumatismes), Lysosomes (anatomopathologie), Lysosomes (métabolisme), Phagosomes (anatomopathologie), Phagosomes (métabolisme), Sepsie (anatomopathologie), Sepsie (métabolisme), Souris.
- MESH :
- analogues et dérivés : Adénine.
- anatomopathologie : Foie, Lysosomes, Phagosomes, Sepsie.
- métabolisme : Foie, Lysosomes, Phagosomes, Sepsie.
- pharmacologie : Adénine, Antiamibiens, Anticonvulsivants, Carbamazépine, Chloroquine.
- traumatismes : Foie.
- Animaux, Autophagie, Souris.
English descriptors
- KwdEn :
- Adenine (analogs & derivatives), Adenine (pharmacology), Amebicides (pharmacology), Animals, Anticonvulsants (pharmacology), Autophagy, Carbamazepine (pharmacology), Chloroquine (pharmacology), Liver (injuries), Liver (metabolism), Liver (pathology), Lysosomes (metabolism), Lysosomes (pathology), Mice, Phagosomes (metabolism), Phagosomes (pathology), Sepsis (metabolism), Sepsis (pathology).
- MESH :
- chemical , analogs & derivatives : Adenine.
- chemical , pharmacology : Adenine, Amebicides, Anticonvulsants, Carbamazepine, Chloroquine.
- injuries : Liver.
- metabolism : Liver, Lysosomes, Phagosomes, Sepsis.
- pathology : Liver, Lysosomes, Phagosomes, Sepsis.
- Animals, Autophagy, Mice.
Abstract
The accumulation of autophagosomes in the terminal step of the autophagic process has recently emerged as a potentially maladaptive process in the septic heart and lung. However, the role of autophagy in the septic liver has not been ascertained. This study was investigated by first examining the entire sequence of the autophagic process in the liver of septic mice. Second, a novel pharmacotherapeutic approach was utilized to treat sepsis with autophagy enhancer/inhibitor. Sepsis was induced by cecal ligation and puncture (CLP). C57BL/6 mice received autophagy enhancer carbamazepine (CBZ), autophagy inhibitor 3-methyladenine (inhibition of autophagosomal formation), or chloroquine (impairment of autophagosomal clearance). We found that the whole autophagic process was activated at 4 h after CLP; however, it did not proceed to completion during the 4- to 24-h time period, as indicated by accumulated autophagosomes and decreased autophagic flux. Carbamazepine, which induced complete activation of the autophagic process, improved CLP survival. This protective effect was also associated with decreased cell death, inflammatory responses, and hepatic injury. However, disruption of autophagosomal clearance with chloroquine abolished the above protective effects in CBZ-treated CLP mice. 3-Methyladenine, which resulted in inhibition of the autophagosomal formation, did not show any above beneficial effects in CLP mice. Impaired autophagosome-lysome fusion resulting in incomplete activation of autophagy may contribute to sepsis-induced liver injury. Treatment with CBZ may serve a protective role in the septic liver, possibly through the effect of complete activation of autophagic process.
DOI: 10.1097/SHK.0000000000000111
PubMed: 24365881
Affiliations:
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Yuan</name></author><author><name sortKey="Hsieh, Ya Ching" sort="Hsieh, Ya Ching" uniqKey="Hsieh Y" first="Ya-Ching" last="Hsieh">Ya-Ching Hsieh</name></author></analytic><series><title level="j">Shock (Augusta, Ga.)</title><idno type="eISSN">1540-0514</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenine (analogs & derivatives)</term><term>Adenine (pharmacology)</term><term>Amebicides (pharmacology)</term><term>Animals</term><term>Anticonvulsants (pharmacology)</term><term>Autophagy</term><term>Carbamazepine (pharmacology)</term><term>Chloroquine (pharmacology)</term><term>Liver (injuries)</term><term>Liver (metabolism)</term><term>Liver (pathology)</term><term>Lysosomes (metabolism)</term><term>Lysosomes (pathology)</term><term>Mice</term><term>Phagosomes (metabolism)</term><term>Phagosomes (pathology)</term><term>Sepsis (metabolism)</term><term>Sepsis (pathology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adénine (analogues et dérivés)</term><term>Adénine (pharmacologie)</term><term>Animaux</term><term>Antiamibiens (pharmacologie)</term><term>Anticonvulsivants (pharmacologie)</term><term>Autophagie</term><term>Carbamazépine (pharmacologie)</term><term>Chloroquine (pharmacologie)</term><term>Foie (anatomopathologie)</term><term>Foie (métabolisme)</term><term>Foie (traumatismes)</term><term>Lysosomes (anatomopathologie)</term><term>Lysosomes (métabolisme)</term><term>Phagosomes (anatomopathologie)</term><term>Phagosomes (métabolisme)</term><term>Sepsie (anatomopathologie)</term><term>Sepsie (métabolisme)</term><term>Souris</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Adenine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adenine</term><term>Amebicides</term><term>Anticonvulsants</term><term>Carbamazepine</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Adénine</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Foie</term><term>Lysosomes</term><term>Phagosomes</term><term>Sepsie</term></keywords><keywords scheme="MESH" qualifier="injuries" xml:lang="en"><term>Liver</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Liver</term><term>Lysosomes</term><term>Phagosomes</term><term>Sepsis</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Foie</term><term>Lysosomes</term><term>Phagosomes</term><term>Sepsie</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Liver</term><term>Lysosomes</term><term>Phagosomes</term><term>Sepsis</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Adénine</term><term>Antiamibiens</term><term>Anticonvulsivants</term><term>Carbamazépine</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="traumatismes" xml:lang="fr"><term>Foie</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Autophagy</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Autophagie</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The accumulation of autophagosomes in the terminal step of the autophagic process has recently emerged as a potentially maladaptive process in the septic heart and lung. However, the role of autophagy in the septic liver has not been ascertained. This study was investigated by first examining the entire sequence of the autophagic process in the liver of septic mice. Second, a novel pharmacotherapeutic approach was utilized to treat sepsis with autophagy enhancer/inhibitor. Sepsis was induced by cecal ligation and puncture (CLP). C57BL/6 mice received autophagy enhancer carbamazepine (CBZ), autophagy inhibitor 3-methyladenine (inhibition of autophagosomal formation), or chloroquine (impairment of autophagosomal clearance). We found that the whole autophagic process was activated at 4 h after CLP; however, it did not proceed to completion during the 4- to 24-h time period, as indicated by accumulated autophagosomes and decreased autophagic flux. Carbamazepine, which induced complete activation of the autophagic process, improved CLP survival. This protective effect was also associated with decreased cell death, inflammatory responses, and hepatic injury. However, disruption of autophagosomal clearance with chloroquine abolished the above protective effects in CBZ-treated CLP mice. 3-Methyladenine, which resulted in inhibition of the autophagosomal formation, did not show any above beneficial effects in CLP mice. Impaired autophagosome-lysome fusion resulting in incomplete activation of autophagy may contribute to sepsis-induced liver injury. Treatment with CBZ may serve a protective role in the septic liver, possibly through the effect of complete activation of autophagic process. </div></front></TEI><affiliations><list><country><li>Taïwan</li></country></list><tree><noCountry><name sortKey="Chang, Ya Fang" sort="Chang, Ya Fang" uniqKey="Chang Y" first="Ya-Fang" last="Chang">Ya-Fang Chang</name><name sortKey="Hsieh, Ya Ching" sort="Hsieh, Ya Ching" uniqKey="Hsieh Y" first="Ya-Ching" last="Hsieh">Ya-Ching Hsieh</name><name sortKey="Kuo, Po Lin" sort="Kuo, Po Lin" uniqKey="Kuo P" first="Po-Lin" last="Kuo">Po-Lin Kuo</name><name sortKey="Lee, Po Huang" sort="Lee, Po Huang" uniqKey="Lee P" first="Po-Huang" last="Lee">Po-Huang Lee</name><name sortKey="Lo, Steven" sort="Lo, Steven" uniqKey="Lo S" first="Steven" last="Lo">Steven Lo</name><name sortKey="Perng, Daw Shyong" sort="Perng, Daw Shyong" uniqKey="Perng D" first="Daw-Shyong" last="Perng">Daw-Shyong Perng</name><name sortKey="Wu, David Bin Chia" sort="Wu, David Bin Chia" uniqKey="Wu D" first="David Bin-Chia" last="Wu">David Bin-Chia Wu</name><name sortKey="Yu, Ming Lung" sort="Yu, Ming Lung" uniqKey="Yu M" first="Ming-Lung" last="Yu">Ming-Lung Yu</name><name sortKey="Yuan, Shyng Shiou F" sort="Yuan, Shyng Shiou F" uniqKey="Yuan S" first="Shyng-Shiou F" last="Yuan">Shyng-Shiou F. Yuan</name></noCountry><country name="Taïwan"><noRegion><name sortKey="Lin, Chih Wen" sort="Lin, Chih Wen" uniqKey="Lin C" first="Chih-Wen" last="Lin">Chih-Wen Lin</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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