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. Author manuscript; available in PMC: 2015 May 1.
Published in final edited form as: J Cardiovasc Pharmacol. 2014 May;63(5):406–411. doi: 10.1097/FJC.0000000000000061

Figure 2.

Figure 2

IL-15 increases cardiomyocyte survival after Hx/Rx and activates the transcription factor STAT3. These effects can be blocked with WP1066 (a STAT3 inhibitor). A. Addition of IL-15 (5 ng/ml) improves survival of CMs during Hx/Rx. WP1066 inhibits this benefit. WP1066 (1 μM) was added to cultures of adult cardiac myocytes after 3 h of hypoxia and just prior to treatment with IL-15 (5 ng/ml) at the onset of 22 h of re-oxygenation. B. Western blot analysis of IL-15 stimulated cardiomyocytes revealed increased STAT3 phosphorylation during normoxia. Activation was two-fold over untreated cardiomyocyte controls. WP1066 added 15 min prior to stimulation with IL-15 (5 ng/ml) for 10 min blocked activation of STAT3 phosphorylation.

Nx, normoxia; Hx/Rx, hypoxia/re-oxygenation; Con, control; WP, WP1066. A: n = 5 per group. *P < 0.05 vs. control and IL-15. B: n = 5 per group. *P < 0.05 vs. IL-15.