Abstract 14465: C1q/TNF-Related Protein-13 (CTRP13) Protects Against Myocardial Injury following Ischemia-Reperfusion via the Phosphatidyl-Inositol 3-Kinase (PI3K) Pathway
Background: C1q/TNF-Related Protein-13 (CTRP13) is a novel insulin sensitizing adipokine by promoting glucose uptake in peripheral tissues. To date, the impact of CTRP13 on the cardiovascular system has not been described. We sought to study the effect of full length CTRP13 (fCTRP13) and globular CTRP13 (gCTRP13) in an ischemic Langendorff perfused rat heart.
Methods: Following global ischemia (30 minutes) and reperfusion (120 minutes), with or without fCTRP13 or gCTRP13 pre-treatment (0.25μg/ml/g/minute), cardiac function and infarct size were measured.
Cardiac function: In an isolated rat heart Langendorff system, we measured left ventricular developed pressure (LVDP) relating to maximal rates of LV pressure decay and dP/dtmin and dP/dtmax (+/-dp/dt), a specific indicator of isovolumetric phase index of left ventricular contractility.
Infarct size: Infarct size was determined by triphenyltetrazolium chloride staining and planimetry of the traced sections.
Results: The control (saline treated) group exhibited poor cardiac functional recovery (Figure 1A) and a significant decline in cardiac function (Figure 1B-C) following global ischemia and reperfusion whence compared to pre-treatment with fCTRP13 or gCTRP13.
Transverse sections of rat hearts showed an increased area of viability (red) following fCTRP13 or gCTRP13 pre-treatment, compared to controls; infarct size was significantly reduced (Figure 2A). The effects of fCTRP13 and gCTRP13 were attenuated by the PI3K inhibitor, wortmannin (10μM) but not the MEK inhibitor, U0126 (10μM) (Figure 2B).
Conclusions: CTRP13 protects against acute cardiac injury following ischemia-reperfusion through the PI3K pathway.
- © 2013 by American Heart Association, Inc.