Key result
Alveolar hypoxia and IL-18 exposure increased protein phosphatase 2A activity to 234% and reduced phospholamban phosphorylation at Ser16 to 54% of control in mice and isolated cardiomyocytes.
Alveolar hypoxia-induced diastolic dysfunction may be mediated by increased circulating IL-18, which upregulates PP2A and reduces phospholamban phosphorylation.
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May link hypoxia to diastolic dysfunction via IL-18/PP2A in mice; leaves open human relevance.
Larsen et al. (2008) studied Alveolar hypoxia and diastolic dysfunction. Alveolar hypoxia (10% oxygen) and IL-18 exposure vs. Control was evaluated on Amount and activity of protein phosphatase (PP) 2A and phosphorylation of phospholamban at Ser16. Alveolar hypoxia and IL-18 exposure increased protein phosphatase 2A activity to 234% and reduced phospholamban phosphorylation at Ser16 to 54% of control in mice and isolated cardiomyocytes.
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