Silencing HMGB1 expression inhibits adriamycin's heart toxicity via TLR4 dependent manner through MAPK signal transduction

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dc.authoridKAYA, Salih Tunc/0000-0002-4133-407X
dc.authorwosidSariman, Melda/AAM-1356-2020
dc.authorwosidSariman, Melda/ABB-8877-2021
dc.contributor.authorTaskin, Eylem
dc.contributor.authorGuven, Celal
dc.contributor.authorKaya, Salih Tunc
dc.contributor.authorSariman, Melda
dc.contributor.authorEmrence, Zeliha
dc.contributor.authorEkmekci, Sema Sirma
dc.contributor.authorAkcakaya, Handan
dc.date.accessioned2021-12-01T18:50:20Z
dc.date.available2021-12-01T18:50:20Z
dc.date.issued2020
dc.department[Belirlenecek]en_US
dc.description.abstractPurpose: Adriamycin (APR) is a commonly used anti-cancer drug. ADR has toxic effects on cardiomyocytes and leads to heart failure. However, the underlying mechanism(s) by which ADR causes heart failure is still not clarified exactly. The aim of present study is to investigate whether ADR-induced heart failure is mediated via HMGB1/TLR4 to initiate the apoptosis through MAPK/AMPK pathways. Methods: H9c2 cell line was used to create four groups as a control, HMGB1 inhibition, ADR, ADR+HMGB1 inhibition. Silencing HMGB1 was performed with specific small interfering RNA. ADR was used at 2 mu M concentration for 36 and 48 hours. Protein and genes expressions, apoptosis was measured. Results: Although ADR decreased AMPK, pAMPK, ERK1/2, pERK1/2, p38, JNK protein expression, ADR+HMGB1 inhibition led to change those protein expressions. The effect of silencing of HMGB1 prevented apoptosis induced by ADR in the cells. HMGB1 caused changes a kind of posttranscriptional modification on the TLR4 receptor. This posttranscriptional modification of TLR4 receptor led to decreased AMPK protein level, but phosphorylated-AMPK. This alternation of AMPK protein caused enhancing of JNK protein, resulting from the decline of p38 and ERK protein levels. Eventually, JNK triggered apoptosis by a caspase-dependent pathway. The number of TUNEL positive and active caspase 8 cells at ADR was high, although HMGB1 silencing could decrease the cell numbers. Conclusions: Inhibition of HMGB1 might prevent the lose of the cardiac cell by inhibition of apoptotic pathway, therefore HMGB1 plays an essential role as amplifying on ADR toxicity on the heart by TLR4.en_US
dc.description.sponsorshipScientific and Technological Research Council of Turkey (TUBITAK)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [114S118]en_US
dc.description.sponsorshipThis study was supported by The Scientific and Technological Research Council of Turkey (TUBITAK) as a Project No: 114S118.en_US
dc.identifier.endpage565en_US
dc.identifier.issn1107-0625
dc.identifier.issn2241-6293
dc.identifier.issue1en_US
dc.identifier.pmid32277683en_US
dc.identifier.scopus2-s2.0-85081558392en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage554en_US
dc.identifier.urihttps://hdl.handle.net/20.500.12684/10861
dc.identifier.volume25en_US
dc.identifier.wosWOS:000517089300076en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherImprimatur Publicationsen_US
dc.relation.ispartofJournal Of Buonen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectadriamycinen_US
dc.subjectHMGB1en_US
dc.subjectAMPKen_US
dc.subjectTLR4en_US
dc.subjectapoptosisen_US
dc.subjectcardiac muscle cellen_US
dc.subjectMitochondrial Dysfunctionen_US
dc.subjectInduced Cardiotoxicityen_US
dc.subjectDoxorubicinen_US
dc.subjectAmpken_US
dc.subjectCellsen_US
dc.subjectLiveren_US
dc.titleSilencing HMGB1 expression inhibits adriamycin's heart toxicity via TLR4 dependent manner through MAPK signal transductionen_US
dc.typeArticleen_US

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