We are analyzing https://link.springer.com/article/10.1007/s00395-005-0537-4.

Title:
Erythropoietin protects the myocardium against reperfusion injury in vitro and in vivo | Basic Research in Cardiology
Description:
Objective Erythropoietin (EPO) is a hormone that is currently used to treat patients with renal failure and anaemia. However, it has also been shown to protect against ischaemia/reperfusion injury; this protection occurring via activation of the ERK 1/2 and PI3K pathways. Since we have previously shown activation of ERK 1/2 and PI3K to be important for protection against reperfusion–induced injury in the myocardium, this study was designed to investigate its effect in the myocardium using both an isolated perfused rat heart and an in vivo rat recovery model of ischaemia–reperfusion. Methods Using an in vitro isolated rat heart model of 35 minutes ischaemia and 2 hours reperfusion, EPO (50 ng/ml) was administered to the rat myocardium 5 minutes prior to reperfusion for 20 minutes. The in vivo open–chest rat model consisted of 40 minutes ischaemia followed by 24 hours reperfusion with EPO (5000 U/kg) being administered at the point of reperfusion. Results In the isolated perfused heart studies 50 ng/ml EPO was found to provide protection with a % I/R of 22.9% ± 6.4 vs 54.5% ± 7.4 for the ischaemic control group. To examine the mechanistic pathways involved in EPO–mediated protection, we co–administered the ERK 1/2 inhibitor, U0126 (10 uM) or the PI3K inhibitors, wortmannin, (100 nM) and LY294002 (15 µM) at reperfusion. U0126, wortmannin and LY294002 all abrogated EPO–mediated protection (% I/R 49.2% ± 5.6, 46.1% ± 5.5 and 49.9% ± 6.1 respectively, p < 0.05). In the in vivo open–chest rat model, the % I/R was significantly attenuated in EPO–treated animals from 53.6 % ± 3.7 in the control to 32.5% +/– 2.9 (p < 0.05). Likewise, wortmannin abrogated EPO–mediated protection (% I/R 50.7 ± 2.3 v EPO 32.5% ± 2.9, p < 0.05). Conclusion We demonstrate that EPO, administered at the point of reperfusion, reduced infarct size in an isolated perfused rat heart, in an ERK and PI3K dependent manner; in addition the mechanism was also confirmed in a whole animal model of ischaemia–reperfusion. These results suggest that EPO may be able to directly protect the myocardium against lethal reperfusion–induced injury and so offer the myocardium an additional clinical advantage over and above its ability to improve the oxygen carrying capacity of the blood.
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Topics {✒️}

month download article/chapter article basic research abrogated epo–mediated protection lethal reperfusion–induced injury related subjects acute ischemia–reperfusion injury full article pdf randomized controlled trial privacy choices/manage cookies adult rat cardiomyocytes van veldhuisen dj growth factor signaling acute cardioprotective effect acute myocardial infarction bradykinin limits infarction chronic renal failure london wc1e 6db hypoxia–induced apoptosis cardioprotective effects epo–mediated protection akt–dependent pathway european economic area scope submit manuscript 50 ng/ml mechanistic pathways involved reduced infarct size additional clinical advantage coronary microvascular dysfunction promotes beneficial remodeling broad neuroprotective activity van der meer van gilst wh de montellano pr coronary artery ligation 8–phenyl–4h–1–benzopyran– 4 neonatal hypoxia–ischemia reperfusion–induced injury pi3k dependent manner conditions privacy policy epo–treated animals reperfusion injury revisited oxygen carrying capacity pritchard ka jr ischemia–reperfusion injury reperfused ischemic heart check access instant access accepting optional cookies ischaemic control group erythropoietin receptor expression

Questions {❓}

Yellon DM, Baxter GF (1999) Reperfusion injury revisited: is there a role for growth factor signaling in limiting lethal reperfusion injury?

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         description:Erythropoietin (EPO) is a hormone that is currently used to treat patients with renal failure and anaemia. However, it has also been shown to protect against ischaemia/reperfusion injury; this protection occurring via activation of the ERK 1/2 and PI3K pathways. Since we have previously shown activation of ERK 1/2 and PI3K to be important for protection against reperfusion–induced injury in the myocardium, this study was designed to investigate its effect in the myocardium using both an isolated perfused rat heart and an in vivo rat recovery model of ischaemia–reperfusion. Using an in vitro isolated rat heart model of 35 minutes ischaemia and 2 hours reperfusion, EPO (50 ng/ml) was administered to the rat myocardium 5 minutes prior to reperfusion for 20 minutes. The in vivo open–chest rat model consisted of 40 minutes ischaemia followed by 24 hours reperfusion with EPO (5000 U/kg) being administered at the point of reperfusion. In the isolated perfused heart studies 50 ng/ml EPO was found to provide protection with a % I/R of 22.9% ± 6.4 vs 54.5% ± 7.4 for the ischaemic control group. To examine the mechanistic pathways involved in EPO–mediated protection, we co–administered the ERK 1/2 inhibitor, U0126 (10 uM) or the PI3K inhibitors, wortmannin, (100 nM) and LY294002 (15 µM) at reperfusion. U0126, wortmannin and LY294002 all abrogated EPO–mediated protection (% I/R 49.2% ± 5.6, 46.1% ± 5.5 and 49.9% ± 6.1 respectively, p < 0.05). In the in vivo open–chest rat model, the % I/R was significantly attenuated in EPO–treated animals from 53.6 % ± 3.7 in the control to 32.5% +/– 2.9 (p < 0.05). Likewise, wortmannin abrogated EPO–mediated protection (% I/R 50.7 ± 2.3 v EPO 32.5% ± 2.9, p < 0.05). We demonstrate that EPO, administered at the point of reperfusion, reduced infarct size in an isolated perfused rat heart, in an ERK and PI3K dependent manner; in addition the mechanism was also confirmed in a whole animal model of ischaemia–reperfusion. These results suggest that EPO may be able to directly protect the myocardium against lethal reperfusion–induced injury and so offer the myocardium an additional clinical advantage over and above its ability to improve the oxygen carrying capacity of the blood.
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