Disruption of erythroid K-Cl cotransporters alters erythrocyte volume and partially rescues erythrocyte dehydration in SAD mice
J. Clin. Invest. Marco B. Rust, et al. 117:1708 doi:10.1172/JCI30630 [Go to this article.]

Figure 4
rbc K-Cl cotransport activity and K⁺ content of SAD mice of various Kcc genotypes. (A–D) K⁺ efflux from rbc measured as described in Methods in the presence of Cl^– or upon its substitution by SFA^–, measured under isotonic or hypotonic conditions and in the presence of 500 mM urea added to the isotonic solutions. Gray bars indicate a significant difference between isotonic and stimulated K⁺ fluxes. Black bars indicate a significant difference between K⁺ fluxes in a single condition in the presence and absence of Cl^–. (A) The elevated isotonic K-Cl cotransport activity of SAD rbc (compare with WT rbc in Figure 2A) was further stimulated by hypotonicity and by urea. Absence of KCC1 had minimal effect on K-Cl cotransport activity (B), whereas absence of KCC3 reduced K-Cl cotransport activity (C), and absence of both KCC1 and KCC3 nearly abolished cotransport activity (D). (E) Disruption of KCC1 and KCC3 did not alter rbc K⁺ content in the absence of the SAD transgene but rescued nearly completely the reduced K⁺ content of SAD rbc. *P ≤ 0.05.