How do sickle cells become dehydrated?

Regulation of K-Cl cotransport by Syk and Src protein tyrosine kinases in deoxygenated sickle cells

“…Dehydration of SS cells results from a net K + loss involving different pathways: K + efflux mediated by imbalance between Na + and K + permeability via the "sickling-induced pathway" (SIP), by KCC and by the Ca 2+ -dependent K + channel (Gardos channel). Recent models have featured primary dehydration via activation of KCC in reticulocytes, with secondary facilitation of sickling and Gardos channel activation, especially in cells lacking fetal haemoglobin [26,34]. A role for KCC in in vivo dehydration of young SS cells has been suggested directly [20] and demonstrated indirectly in SAD mice and human patients from the increase in the red cell hydration state induced by oral Mg 2+ supplementation [12,13].…”

Structural Validation and Homology Modeling of Differentially Expressed Proteins in Rattus Norvergicus Induced by Bisphenol a and Probiotic Treatement.

“…More recent data indicate a direct participation of the vascular endothelium, of multiple and complex cellular interactions, and of a global inflammation-mediated cell activation, in the initiation and propagation of the vaso-occlusive process with two consecutive steps. The first step involves adhesion of the stress reticulocytes [23] and activated polymorphonuclear neutrophils8 , (iii) signalling pathways in the red blood ( the signalling pathways in the red blood cell, makes the cell susceptible to be modulated by stress, hypoxia, and by the inflammatory response and to influence the activation status of adhesion receptors and of ion transporters implicated in SS-RBC dehydration and finally of a syndrome of complex endothelial dysfunction involving abnormalities of the metabolism of nitric oxide (NO) )was brought into light to the endothelium of post-capillary veinules, slowing down the blood flow and thereby inducing and propagating sickling of mature SS-RBCs that are maintained for a longer time in a hypoxic environment and activates polymorphonuclear neutrophils second step involves the entrapment of irreversible sickle cells and to the complete occlusion of the micro-vessels [24][25][26][27][28][29][30][31] Conclusion:-…”