Key result
TNFalpha (10-50 ng/mL) stimulated (86)Rb efflux, depressed KCl-stimulated (45)Ca uptake, and inhibited insulin-stimulated (3)H-deoxyglucose uptake in H9c2 cardiomyocytes.
TNFalpha modulates ion fluxes and glucose uptake in H9c2 cardiomyocytes, suggesting adaptive and protective effects during environmental injury.
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Suggests TNFα may confer adaptive cardiomyocyte protection; hypothesis-generating and requires in vivo validation before clinical relevance.
Tumor necrosis factor (TNFalpha) is an inflammatory cytokine that induces programmed cell death in a variety of tissue types, including the heart. Recent experimental data suggest that the TNF expressed within the myocardium in response to environmental injury plays an important role in initiating homeostatic response. The effect of TNFalpha (10-50 ng/mL) was studied on (86)Rb efflux, (3)H-deoxyglucose uptake, or (45)Ca uptake in H9c2 cardiomyocytes. TNFalpha stimulated (86)Rb efflux from cultures, while 2 micro M glibenclamide blocker of ATP-sensitive potassium channels or 20 micro M zvad-fmk caspase inhibitor attenuated this effect. TNFalpha also depressed the stimulatory effect of 80 mM KCl on (45)Ca uptake in the cardiomyocytes. TNFalpha inhibited the stimulatory effect of 100 nM insulin on (3)H-deoxyglucose uptake. Our findings further suggest that TNFalpha mediated adaptive and protective effects in the heart during a brief environmental injury.
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El‐Ani et al. (2003) studied H9c2 cardiomyocytes. TNFalpha was evaluated on (86)Rb efflux, (3)H-deoxyglucose uptake, and (45)Ca uptake. TNFalpha (10-50 ng/mL) stimulated (86)Rb efflux, depressed KCl-stimulated (45)Ca uptake, and inhibited insulin-stimulated (3)H-deoxyglucose uptake in H9c2 cardiomyocytes.
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