Figure 4
Iron homeostasis in failing human hearts. (A) Total iron and (B) non-haem iron concentration in LV tissue samples from individuals who died from non-cardiac causes (Con, n = 18) and from failing hearts (F) with ischaemic (ICM, n = 11) or dilated aetiology (DCM, n = 10). (C) HAMP mRNA expression (normalized to GAPDH) in LV tissue samples from Con, F, ICM, and DCM; n = 9–11. (D–F) Representative immunoblot and summary data showing ferroportin (FPN), GAPDH, and Na+K+ATPase protein expression in whole cell lysates and membrane fractions of LV tissue samples from Con, ICM, and DCM; n = 9–10. GAPDH was used as loading control for whole cell lysates and as a cytosolic protein marker for membrane fractions. Na+K+ATPase was used as a membrane protein marker and loading control for membrane fraction immunoblots. *P < 0.05, **P < 0.01, ***P < 0.001; Kruskal–Wallis test with Dunn’s multiple comparisons.

Iron homeostasis in failing human hearts. (A) Total iron and (B) non-haem iron concentration in LV tissue samples from individuals who died from non-cardiac causes (Con, n = 18) and from failing hearts (F) with ischaemic (ICM, n = 11) or dilated aetiology (DCM, n = 10). (C) HAMP mRNA expression (normalized to GAPDH) in LV tissue samples from Con, F, ICM, and DCM; n = 9–11. (D–F) Representative immunoblot and summary data showing ferroportin (FPN), GAPDH, and Na+K+ATPase protein expression in whole cell lysates and membrane fractions of LV tissue samples from Con, ICM, and DCM; n = 9–10. GAPDH was used as loading control for whole cell lysates and as a cytosolic protein marker for membrane fractions. Na+K+ATPase was used as a membrane protein marker and loading control for membrane fraction immunoblots. *P < 0.05, **P < 0.01, ***P < 0.001; Kruskal–Wallis test with Dunn’s multiple comparisons.

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