Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6273069 | Neuroscience | 2015 | 9 Pages |
Abstract
The results showed that heat stress led to Hsp70 overexpression which rendered neuroprotection after ischemia-like injury. Overexpression Hsp70 also interrupts the phosphorylation of IκB, JNK and p38 and blunts DNA binding of their transcription factors (NF-κB, AP-1 and STAT-1), effectively downregulating the expression of pro-inflammatory genes in heat-pretreated astrocytes. Taken together, these results suggest that overexpression of Hsp70 may protect against brain ischemia via an anti-inflammatory mechanism by interrupting the phosphorylation of upstream of transcription factors.
Keywords
NF-κBSTAT-170-kDa heat shock proteinBSSAP-1MCAOOGDIκBIL-1βhsp70RT-PCRJnkc-Jun N-terminal kinasesJAKsIschemic injuryinflammationmiddle cerebral artery occlusionInterleukin-1 betaEnzyme-linked immunosorbent assayELISAtumor necrosis factor alphaEMSA یا electrophoretic mobility shift assay Transcription factorsTNF-αnuclear factor-κBPhosphorylationOxygen and glucose deprivationbalanced salt solutioninhibitor of κBreverse transcription-polymerase chain reactionactivator protein-1Janus kinases
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Authors
J.Y. Kim, M.A. Yenari, J.E. Lee,