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Activated STAT3 is induced following I/R
Fig. 3.
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To confirm that endogenous STAT3 activity was enhanced following I/R, we carried out our Ly6E STAT3 responsive reporter assay and showed that there was a significant increase (40-fold) in Ly6E promoter activity in NRVM G-749 exposed to I/R (Fig. 3C). Furthermore we also demonstrate that two well known STAT3 responsive genes SOCS3 [25] and c-Fos [26] were also upregulated in NRVM cells exposed to I/R as assessed by qPCR (Fig. 3D). As a positive control we also transduced NRVM with a constitutively active STAT3 adenovirus (Ad-STAT3C) [27] and showed that enhanced levels of STAT3 activity was also associated with upregulation of SOCS3 and c-Fos mRNAs (Fig. 3E). Taken together, these data strongly suggests that endogenous STAT3 does indeed become activated and induces a transcriptional programme that may modulate the levels of I/R-cell death in cardiac cells.





 
 
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