Author + information
- Jeong-Su Kim,
- Ju-Hyun Park,
- Kook-Jin Chun,
- Young-Ho Jang,
- June-Hong Kim,
- Yong-Hyun Park,
- Jun Kim,
- Chang-Bae Sohn,
- Sang-Hyun Lee,
- Kyeong-Won Yun and
- Jin-Hee Choi
We hypothesized that the SDF-1α/CXCR4 signaling pathway is directly involved in the cardioprotective effect of IPOC.
Materials and Method
Isolated rat hearts were subjected to 30-min of regional ischemia and 2-h of reperfusion. IPOC was induced by 6 cycles each of 10-sec reperfusion and 10-sec global ischemia. CXCR4 antagonist, AMD3100 was applied in IPOC-induced hearts. Infarct size was assessed. The SDF-1α and cardiac enzymes concentrations were determined. The phosphorylation states of ERK1/2 and Akt was determined.
SDF-1a concentration in IPOC group were significantly higher than other groups (p=0.0029). IPOC significantly reduced infarct size from 29.3 ± 8.4% to 17.8 ± 7.0% of the risk area (p = 0.022 vs. CON). AMD3100 attenuated the infarct reducing effect by IPOC (28.5 ± 8.9 %, p = 0.045 vs. IPOC). LDH and CL levels were significantly lower in the IPOC group and these effects were reversed by AMD3100 (p=0.009 and p=0.0321, respectively). ERK1/2 and Akt phosphorylation was increased by IPOC (226.1 ± 71.8%; p = 0.01 vs. CON and 296.4 ± 93.1%; p = 0.02 vs. CON, respectively) and this totally blocked by AMD3100 (83.8 ± 28.0%; p = 0.02 vs. IPOC and 138.3 ± 28.5%; p = 0.009 vs. IPOC, respectively).
SDF-1α/CXCR4 signaling may be involved in the cardioprotection by IPOC and this signaling pathway couples to the ERK1/2 and Akt pathways.
Poster Sessions, Expo North
Monday, March 11, 2013, 9:45 a.m.-10:30 a.m.
Session Title: Acute Coronary Syndromes: Basic V
Abstract Category: 2. Acute Coronary Syndromes: Basic
Presentation Number: 1300-193
- 2013 American College of Cardiology Foundation