Nitric oxide inhibits autophagy via suppression of JNK in meniscal cells

Basit Öğe Kaydı
dc.contributor.authorShen, Chao
dc.contributor.authorYan, Jun
dc.contributor.authorErkocak, Omer Faruk
dc.contributor.authorZheng, Xin-Feng
dc.contributor.authorChen, Xiao-Dong
dc.date.accessioned2020-03-26T18:51:45Z
dc.date.available2020-03-26T18:51:45Z
dc.date.issued2014
dc.departmentSelçuk Üniversitesien_US
dc.description.abstractObjective. Autophagy is a potential protective mechanism that is involved in several degenerative diseases. Nitric oxide (NO) is associated with programmed cellular death in meniscal cells, but whether it can induce autophagy is still undetermined. This study aims to investigate the interaction between autophagy and NO in normal human meniscal cells. Methods. Normal meniscal cells were harvested from female patients. NO donors and NO synthase inhibitors were used to regulate the level of NO. Changes in the incidence of autophagy and apoptosis were examined using flow cytometry, western blot and immunofluorescence methods. The effects of NO-mediated autophagy regulation of the expression of MMPs and aggrecanases (ADAMTS-4 and -5) were analysed by real-time PCR. Results. NO donors inhibited autophagy as well as augmented apoptosis in human meniscal cells with serum deprivation. Conversely, treatment with NOS inhibitors resulted in up-regulation of the autophagy level while repressing apoptosis. NOS inhibitor treatment also resulted in down-regulation of MMPs and aggrecanase mRNA expression. This effect of NOS inhibitor was also blocked by autophagy inhibitors. Our results also showed that NOS inhibitor enhanced Jun-N-terminal kinase (JNK) activation. Furthermore, SP600125, a selective JNK inhibitor, blocked up-regulation of autophagy by NOS inhibitor. Conclusion. Our results demonstrated that NO augmented serum deprivation-induced apoptosis of meniscal cells via inhibition of autophagy through inactivation of JNK. Up-regulation of autophagy may be a potential approach in the treatment of meniscal tissue degeneration.en_US
dc.description.sponsorshipNational Natural Science Foundation of ChinaNational Natural Science Foundation of China [81101379, 81171705, 81000793]; Natural Science Fund of the Shanghai Jiao Tong University School of Medicine [11XJ21022]en_US
dc.description.sponsorshipThis study was supported by the National Natural Science Foundation of China (81101379, 81171705, 81000793) and the Natural Science Fund of the Shanghai Jiao Tong University School of Medicine (11XJ21022).en_US
dc.identifier.doi10.1093/rheumatology/ket471en_US
dc.identifier.endpage1033en_US
dc.identifier.issn1462-0324en_US
dc.identifier.issn1462-0332en_US
dc.identifier.issue6en_US
dc.identifier.pmid24501244en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage1022en_US
dc.identifier.urihttps://dx.doi.org/10.1093/rheumatology/ket471
dc.identifier.urihttps://hdl.handle.net/20.500.12395/31022
dc.identifier.volume53en_US
dc.identifier.wosWOS:000336982600009en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherOXFORD UNIV PRESSen_US
dc.relation.ispartofRHEUMATOLOGYen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.selcuk20240510_oaigen_US
dc.subjectmeniscusen_US
dc.subjectautophagyen_US
dc.subjectapoptosisen_US
dc.subjectJNKen_US
dc.titleNitric oxide inhibits autophagy via suppression of JNK in meniscal cellsen_US
dc.typeArticleen_US

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