Limits...
Remote ischemic preconditioning of cardiomyocytes inhibits the mitochondrial permeability transition pore independently of reduced calcium-loading or sarcKATP channel activation.

Turrell HE, Thaitirarot C, Crumbie H, Rodrigo G - Physiol Rep (2014)

Bottom Line: However, only conventional-IPC reduced the Ca(2+)-loading during metabolic inhibition and this was independent of any change in sarcKATP channel activity but was associated with a reduction in Na(+)-loading, reflecting a decrease in Na/H exchanger activity.These data show that remote-IPC inhibits MPT pore opening to a similar degree as conventional IPC, however, the contribution of MPT pore inhibition to protection against reperfusion injury is independent of Ca(2+)-loading in remote IPC.We suggest that inhibition of the MPT pore and not Ca(2+)-loading is the common link in cardioprotection between conventional and remote IPC.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiovascular Sciences, University of Leicester, Glenfield General Hospital, Leicester, UK.

No MeSH data available.


Related in: MedlinePlus

Ischemic preconditioning protects myocytes against simulated ischemia/reperfusion injury. (A) Fluorescent images of isolated ventricular myocyte stained with calcein (green) and propidium iodide (red) to indicate viable and necrotic cells, following 30 min of simulated ischemia and 10 min of reperfusion. (B) Mean data expressed as percentage necrotic cells (PI positive) for control naïve myocytes (n = 13; 8, black), conventional IPC myocytes (n = 7; 32, dark gray), and remote IPC myocytes (12; 17, light gray). Mean ± SEM; *P < 0.05, **P < 0.01, one‐way ANOVA followed by Tukey's post hoc test for significance.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4255825&req=5

fig02: Ischemic preconditioning protects myocytes against simulated ischemia/reperfusion injury. (A) Fluorescent images of isolated ventricular myocyte stained with calcein (green) and propidium iodide (red) to indicate viable and necrotic cells, following 30 min of simulated ischemia and 10 min of reperfusion. (B) Mean data expressed as percentage necrotic cells (PI positive) for control naïve myocytes (n = 13; 8, black), conventional IPC myocytes (n = 7; 32, dark gray), and remote IPC myocytes (12; 17, light gray). Mean ± SEM; *P < 0.05, **P < 0.01, one‐way ANOVA followed by Tukey's post hoc test for significance.

Mentions: Data are presented as mean of the experimental observations ± SEM, with the number of hearts and experimental observation indicated as (n = hearts; experiments). For calculations of percent necrotic cells (Fig. 2), the mean from four randomly selected fields‐of‐view containing >100 cells per experimental observation counted and the mean of this mean reported. For calculation of Fura‐2 ratio and percentage Fura‐2 ratio <2.0, the mean from a field‐of‐view containing 8–12 cells per experimental observation was calculated and for recovery of contractile function the mean from a field‐of‐view containing 15–20 cells calculated, and the mean of these mean reported (Fig. 3). Statistical significance was determined using a one‐way ANOVA with Tukey's post hoc test using GraphPad Prism5. P <0.05 were considered statistically significant.


Remote ischemic preconditioning of cardiomyocytes inhibits the mitochondrial permeability transition pore independently of reduced calcium-loading or sarcKATP channel activation.

Turrell HE, Thaitirarot C, Crumbie H, Rodrigo G - Physiol Rep (2014)

Ischemic preconditioning protects myocytes against simulated ischemia/reperfusion injury. (A) Fluorescent images of isolated ventricular myocyte stained with calcein (green) and propidium iodide (red) to indicate viable and necrotic cells, following 30 min of simulated ischemia and 10 min of reperfusion. (B) Mean data expressed as percentage necrotic cells (PI positive) for control naïve myocytes (n = 13; 8, black), conventional IPC myocytes (n = 7; 32, dark gray), and remote IPC myocytes (12; 17, light gray). Mean ± SEM; *P < 0.05, **P < 0.01, one‐way ANOVA followed by Tukey's post hoc test for significance.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4255825&req=5

fig02: Ischemic preconditioning protects myocytes against simulated ischemia/reperfusion injury. (A) Fluorescent images of isolated ventricular myocyte stained with calcein (green) and propidium iodide (red) to indicate viable and necrotic cells, following 30 min of simulated ischemia and 10 min of reperfusion. (B) Mean data expressed as percentage necrotic cells (PI positive) for control naïve myocytes (n = 13; 8, black), conventional IPC myocytes (n = 7; 32, dark gray), and remote IPC myocytes (12; 17, light gray). Mean ± SEM; *P < 0.05, **P < 0.01, one‐way ANOVA followed by Tukey's post hoc test for significance.
Mentions: Data are presented as mean of the experimental observations ± SEM, with the number of hearts and experimental observation indicated as (n = hearts; experiments). For calculations of percent necrotic cells (Fig. 2), the mean from four randomly selected fields‐of‐view containing >100 cells per experimental observation counted and the mean of this mean reported. For calculation of Fura‐2 ratio and percentage Fura‐2 ratio <2.0, the mean from a field‐of‐view containing 8–12 cells per experimental observation was calculated and for recovery of contractile function the mean from a field‐of‐view containing 15–20 cells calculated, and the mean of these mean reported (Fig. 3). Statistical significance was determined using a one‐way ANOVA with Tukey's post hoc test using GraphPad Prism5. P <0.05 were considered statistically significant.

Bottom Line: However, only conventional-IPC reduced the Ca(2+)-loading during metabolic inhibition and this was independent of any change in sarcKATP channel activity but was associated with a reduction in Na(+)-loading, reflecting a decrease in Na/H exchanger activity.These data show that remote-IPC inhibits MPT pore opening to a similar degree as conventional IPC, however, the contribution of MPT pore inhibition to protection against reperfusion injury is independent of Ca(2+)-loading in remote IPC.We suggest that inhibition of the MPT pore and not Ca(2+)-loading is the common link in cardioprotection between conventional and remote IPC.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiovascular Sciences, University of Leicester, Glenfield General Hospital, Leicester, UK.

No MeSH data available.


Related in: MedlinePlus