ORCID Profile
0000-0002-8913-1757
Current Organisation
UNIVERSIDAD DE CHILE
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Publisher: Springer Science and Business Media LLC
Date: 04-05-2021
Publisher: SciELO Agencia Nacional de Investigacion y Desarrollo (ANID)
Date: 03-2011
Publisher: Springer Science and Business Media LLC
Date: 20-01-2006
Abstract: We set out to identify molecular mechanisms underlying the onset of necrotic Ca(2+) overload, triggered in two epithelial cell lines by oxidative stress or metabolic depletion. As reported earlier, the overload was inhibited by extracellular Ca(2+) chelation and the cation channel blocker gadolinium. However, the surface permeability to Ca(2+) was reduced by 60%, thus discarding a role for Ca(2+) channel/carrier activation. Instead, we registered a collapse of the plasma membrane Ca(2+) ATPase (PMCA). Remarkably, inhibition of the Na(+)/K(+) ATPase rescued the PMCA and reverted the Ca(2+) rise. Thermodynamic considerations suggest that the Ca(2+) overload develops when the Na(+)/K(+) ATPase, by virtue of the Na(+) overload, cl s the ATP phosphorylation potential below the minimum required by the PMCA. In addition to providing the mechanism for the onset of Ca(2+) overload, the crosstalk between cation pumps offers a novel explanation for the role of Na(+) in cell death.
Publisher: Springer International Publishing
Date: 2022
Location: No location found
Location: Argentina
Location: Chile
Location: Chile
No related grants have been discovered for Steffen Härtel.