Full metadata record
DC FieldValueLanguage
dc.contributor.authorMa, Wenhan-
dc.contributor.authorZhang, Jingbo-
dc.contributor.authorGuo, Linlin-
dc.contributor.authorWang, Ya-
dc.contributor.authorLu, Shuai-
dc.contributor.authorWang, ZhaoHui-
dc.contributor.authorLu, Qinghua-
dc.contributor.authorWei, Fengtao-
dc.date.accessioned2019-05-20T11:24:35Z-
dc.date.available2019-05-20T11:24:35Z-
dc.date.issued2019-01-24-
dc.identifier.issn1611-2156-
dc.identifier.urihttp://hdl.handle.net/2003/38056-
dc.identifier.urihttp://dx.doi.org/10.17877/DE290R-20039-
dc.description.abstractMacrophages are important mediators of inflammatory cardiovascular diseases, and various macrophage phenotypes exert opposite effects during inflammation. In our previous study, we proved that suppressed androgen receptor (AR) alleviated inflammation during experimental autoimmune myocarditis (EAM). As anti-inflammatory cells, whether M2 macrophages are involved in this process remains unclear. Here, we showed that anti-inflammatory cytokines and M2 macrophages were elevated when AR was suppressed during EAM. In IL-4 stimulationinduced M2 macrophages, impaired AR with ASC-J9 increased the expression of M2 macrophage-related factors. Moreover, suppressed AR expression resulted in macrophage M2 polarization by reducing SOCS3 production and enhancing STAT3 activation. Taken together, our data suggest that AR plays a critical role in macrophage polarization and suppressed redundant AR expression promotes anti-inflammatory M2 macrophages reprogramming. This study suggests a potential therapeutic agent for inflammatory cardiomyopathy through the use of ASC-J9.en
dc.language.isoen-
dc.relation.ispartofseriesEXCLI Journal;Vol. 18 2019-
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/-
dc.subjectMyocarditisen
dc.subjectInflammationen
dc.subjectAndrogen receptoren
dc.subjectM2 macrophagesen
dc.subjectSOCS3en
dc.subjectSTAT3en
dc.subject.ddc610-
dc.titleSuppressed androgen receptor expression promotes M2 macrophage reprogramming through the STAT3/SOCS3 pathwayen
dc.typeText-
dc.type.publicationtypearticle-
dcterms.accessRightsopen access-
eldorado.dnb.zdberstkatid2132560-1-
eldorado.secondarypublicationtrue-
Appears in Collections:Original Articles

Files in This Item:
File Description SizeFormat 
Wei_24012019_proof.pdfDNB533.33 kBAdobe PDFView/Open


This item is protected by original copyright



All resources in the repository are protected by copyright.