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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
Published on: September 18, 2017
Endogenous glycogen prevents Ca2+ overload and hypercontracture in harp seal myocardial cells during simulated
Thale Henden1, Ellen Aasum, Lars Folkow
1Department of Medical Physiology, Faculty of Medicine, Institute of Medical Biology, University of Tromsø, Tromsø N 9037, Norway. thale@fagmed.uit.no
Insights
Elevated myocardial glycogen stores in harp seals protect cardiomyocytes from injury during low oxygen conditions by supporting glycolysis and preventing calcium overload, unlike in rat cells.
Area of Science:
- Cardiology
- Cell Biology
- Biochemistry
Background:
- Myocardial ischemia can lead to cellular injury due to energy depletion and calcium overload.
- Glycogen stores within cardiomyocytes are a potential endogenous energy source during ischemic events.
- Harp seals possess significantly higher myocardial glycogen content compared to other mammals like rats.
Purpose of the Study:
- To investigate if elevated myocardial glycogen content in harp seal cardiomyocytes can prevent calcium (Ca2+) overload and subsequent injury under conditions of low oxygen and limited exogenous substrates.
- To compare the response of harp seal cardiomyocytes to ischemia with that of rat cardiomyocytes, which have lower glycogen stores.
Main Methods:
- Isolated harp seal and rat cardiomyocytes were subjected to simulated ischemia (oxygen and substrate deprivation) for 1 hour.
- Measurements included glycogen content, lactate production, cellular adenosine triphosphate (ATP) levels, total cellular Ca2+ content, and cell morphology (percentage of rod-shaped cells).
- Glycolysis inhibition was assessed using iodoacetate (IAA) in seal cardiomyocytes.
Main Results:
- Seal cardiomyocytes had ~10 times more glycogen than rat cardiomyocytes and exhibited higher lactate production during ischemia.
- Cellular ATP was well-maintained in ischemic seal cardiomyocytes, while rat cardiomyocytes showed a 65% decline.
- Ischemia did not affect total Ca2+ content in seal cardiomyocytes, whereas it increased in rat cardiomyocytes.
- Cell morphology remained unaffected in seal cardiomyocytes but deteriorated in rat cardiomyocytes.
- Inhibition of glycolysis in seal cardiomyocytes under ischemia led to ATP depletion and morphological changes, similar to rat cardiomyocytes.
Conclusions:
- Harp seal cardiomyocytes exhibit superior tolerance to low oxygen conditions compared to rat cardiomyocytes.
- This enhanced tolerance is attributed to a higher rate of glycolysis, fueled by substantial myocardial glycogen reserves.
- Elevated glycogen stores play a crucial role in preventing Ca2+ overload and maintaining cellular integrity during myocardial ischemia.
Abstract:
The purpose of this study was to determine if elevated myocardial glycogen content could obviate Ca(2+) overload and subsequent myocardial injury in the setting of low oxygen and diminished exogenous substrate supplies. Isolated harp seal cardiomyocytes, recognized as having large glycogen stores, were incubated under conditions simulating ischemia (oxygen and substrate deprivation) for 1 h. Rat cardiomyocytes were used for comparison. Freshly isolated seal cardiomyocytes contained approximately 10 times more glycogen than those from rats (479 +/- 39 vs. 48 +/- 5 nmol glucose/mg dry weight (dry wt), mean +/- S.E., n = 6), and during ischemia lactate production was significantly greater in seal compared to rat cardiomyocytes (660 +/- 99 vs. 97 +/- 14 nmol/mg dry wt), while glycogen content decreased both in seal (from 479 +/- 39 to 315 +/- 58 nmol glucose/mg dry wt) and rat cardiomyocytes (from 48 +/- 5 to 18 +/- 5 nmol glucose/mg dry wt). Cellular ATP was well maintained in ischemic seal cardiomyocytes, whereas it showed a 65% decline (from 31 +/- 3 to 11 +/- 1 nmol ATP/mg dry wt) in rat cardiomyocytes. Similarly, total seal cardiomyocyte Ca(2+) content was not affected by ischemia, while Ca(2+) increased from 8.5 +/- 2.0 to 13.3 +/- 2.0 nmol/mg dry wt in ischemic rat myocytes. Rat cardiomyocytes also showed a notable decline in the percentage of rod-shaped cells in response to ischemia (from 66 +/- 4% to 30 +/- 3%), and cell morphology was unaffected in seal incubations. Addition of iodoacetate (IAA, an inhibitor of glycolysis) to seal cardiomyocytes, on top of substrate and oxygen deprivation, reduced the cellular content of ATP by 52.9 +/- 4.4% (from 25 +/- 4 to 11 +/- 2 nmol ATP/mg dry wt) and the percentage of rod-shaped myocytes from 51 +/- 3% to 28 +/- 4%, while total Ca(2+) content was unchanged by these conditions. Seal cardiomyocytes thus tolerate low oxygen conditions better than rat cardiomyocytes. This finding is most likely due to a higher glycolysis rate in seals, fueled by larger myocardial glycogen stores.
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