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. 2010 May 24;88(1):168–178. doi: 10.1093/cvr/cvq151

Figure 2.

Figure 2

Role of miR-21 in preconditioning-induced cytoprotection. (A) PCMY showed up-regulated expression of miR-21 when compared with non-PCMY which was abolished by pre-treatment of the cells with 50 µM PD98059. (B) LDH release assay from various treatment groups of cells. Prior transfection with anti-miR-21 resulted in significant abrogation of the cytoprotective effects of preconditioning in PCMY under oxidant stress when compared with PCMY without anti-miR-21 transfection (P < 0.01). LDH leakage from anti-miR-21-transfected PCMY under oxidant stress was similar to non-PCMY (P < 0.5; n = 3). (C) Western blots showing higher activation of Erk1/2 and pStat3 in PCMY when compared with non-PCMY and remained unaffected after transfection with anti-miR-21 prior to preconditioning of the cells. (D) Treatment with rIL-11 protein significantly increased miR-21 expression in MY (P < 0.001 vs. non-treated control cells; n = 3). Prior treatment of the cells with IL-11Rα-specific antibody, PD098059, or Wortmannin abolished miR-21 expression in the cells upon subsequent treatment with rIL-11. However, simultaneous treatment with PD098059 and Wortmannin was more effective in abolishing IL-11-induced miR-21. (E) Caspase activity was significantly lower in PCMY under anoxic culture conditions (P < 0.001 vs. non-PCMY; n = 3). However, prior treatment with anti-miR-21 abolished the effects of preconditioning and significantly increased caspase activity was observed in PCMY under anoxic culture conditions.