Impact of NF-κB pathway on the apoptosis-inflammation-autophagy crosstalk in human degenerative nucleus pulposus cells
Identifieur interne : 000747 ( Main/Exploration ); précédent : 000746; suivant : 000748Impact of NF-κB pathway on the apoptosis-inflammation-autophagy crosstalk in human degenerative nucleus pulposus cells
Auteurs : Weiwei Yi [République populaire de Chine] ; Yafeng Wen [République populaire de Chine] ; Fuqiang Tan [République populaire de Chine] ; Xi Liu [République populaire de Chine] ; Haiyang Lan [République populaire de Chine] ; He Ye [République populaire de Chine] ; Bo Liu [République populaire de Chine]Source :
- Aging (Albany NY) [ 1945-4589 ] ; 2019.
Abstract
The NF-κB pathway has been reported to play a very important role in the process of intervertebral disc degeneration (IVDD). Our results demonstrated that knockdown of NF-κB with P65-siRNA can significantly decrease cell apoptosis and the expression of pro-inflammation factors TNF-α and IL-1β in LPS-induced nucleus pulposus cells (NPCs). However, the molecular mechanism of NF-κB pathway exerting anti-inflammation and anti-apoptosis function remains unclear. Some researchers reported that inhibiting NF-κB pathway can attenuate the catabolic effect by promoting autophagy during inflammatory conditions in rat nucleus pulposus cells. Therefore, we hypothesized that in human NPCs, inhibiting NF-κB pathway may also promote autophagy. Our results indicated that after knockdown of NF-κB, the autophagy was significantly increased and the expression of p-AKT and p-mTOR protein markedly decreased, but the level of autophagy was inhibited after treatment with AKT activator SC79, suggesting the involvement of AKT/mTOR–mediated autophagy was under autophagy activation. However, both LPS-induced NPCs apoptosis and expression of pro-inflammation factors were further increased by pretreatment with the autophagy inhibitor chloroquine (CQ). These suggested that inhibiting NF-κB pathway can promote autophagy and decrease apoptosis and inflammation response in LPS-induced NPCs. Meanwhile, autophagy triggered by NF-κB inhibition plays a protective role against apoptosis and inflammation.
Url:
DOI: 10.18632/aging.102266
PubMed: 31518335
PubMed Central: 6756901
Affiliations:
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first="Yafeng" last="Wen">Yafeng Wen</name><affiliation wicri:level="1"><nlm:aff id="aff1">Department of Orthopaedic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Orthopaedic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author><author><name sortKey="Tan, Fuqiang" sort="Tan, Fuqiang" uniqKey="Tan F" first="Fuqiang" last="Tan">Fuqiang Tan</name><affiliation wicri:level="1"><nlm:aff id="aff2">Department of Orthopaedic Surgery, Hechuan District People's Hospital of Chongqing, Chongqing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Orthopaedic Surgery, Hechuan District People's Hospital of Chongqing, 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Orthopaedic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author><author><name sortKey="Ye, He" sort="Ye, He" uniqKey="Ye H" first="He" last="Ye">He Ye</name><affiliation wicri:level="1"><nlm:aff id="aff1">Department of Orthopaedic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Orthopaedic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Bo" sort="Liu, Bo" uniqKey="Liu B" first="Bo" last="Liu">Bo Liu</name><affiliation wicri:level="1"><nlm:aff id="aff1">Department of Orthopaedic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Orthopaedic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author></analytic><series><title level="j">Aging (Albany NY)</title><idno type="eISSN">1945-4589</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The NF-κB pathway has been reported to play a very important role in the process of intervertebral disc degeneration (IVDD). Our results demonstrated that knockdown of NF-κB with P65-siRNA can significantly decrease cell apoptosis and the expression of pro-inflammation factors TNF-α and IL-1β in LPS-induced nucleus pulposus cells (NPCs). However, the molecular mechanism of NF-κB pathway exerting anti-inflammation and anti-apoptosis function remains unclear. Some researchers reported that inhibiting NF-κB pathway can attenuate the catabolic effect by promoting autophagy during inflammatory conditions in rat nucleus pulposus cells. Therefore, we hypothesized that in human NPCs, inhibiting NF-κB pathway may also promote autophagy. Our results indicated that after knockdown of NF-κB, the autophagy was significantly increased and the expression of p-AKT and p-mTOR protein markedly decreased, but the level of autophagy was inhibited after treatment with AKT activator SC79, suggesting the involvement of AKT/mTOR–mediated autophagy was under autophagy activation. However, both LPS-induced NPCs apoptosis and expression of pro-inflammation factors were further increased by pretreatment with the autophagy inhibitor chloroquine (CQ). These suggested that inhibiting NF-κB pathway can promote autophagy and decrease apoptosis and inflammation response in LPS-induced NPCs. Meanwhile, autophagy triggered by NF-κB inhibition plays a protective role against apoptosis and inflammation.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Yi, Weiwei" sort="Yi, Weiwei" uniqKey="Yi W" first="Weiwei" last="Yi">Weiwei Yi</name></noRegion><name sortKey="Lan, Haiyang" sort="Lan, Haiyang" uniqKey="Lan H" first="Haiyang" last="Lan">Haiyang Lan</name><name sortKey="Liu, Bo" sort="Liu, Bo" uniqKey="Liu B" first="Bo" last="Liu">Bo Liu</name><name sortKey="Liu, Xi" sort="Liu, Xi" uniqKey="Liu X" first="Xi" last="Liu">Xi Liu</name><name sortKey="Tan, Fuqiang" sort="Tan, Fuqiang" uniqKey="Tan F" first="Fuqiang" last="Tan">Fuqiang Tan</name><name sortKey="Wen, Yafeng" sort="Wen, Yafeng" uniqKey="Wen Y" first="Yafeng" last="Wen">Yafeng Wen</name><name sortKey="Ye, He" sort="Ye, He" uniqKey="Ye H" first="He" last="Ye">He Ye</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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