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Abnormal permeability pathways in human red blood cells.
Blood Cells Mol Dis. 2007 Jul-Aug; 39(1):1-6.BC

Abstract

A number of situations that result in abnormal permeability pathways in human red blood cells (RBCs) have been investigated. In sickle cell disease (SCD), RBCs contain HbS, rather than the normal HbA. When deoxygenated, an abnormal conductance pathway, termed P(sickle), is activated, which contributes to cell dehydration, largely through allowing Ca(2+) entry and subsequent activation of the Gardos channel. Whole-cell patch-clamp recordings from sickle RBCs show a deoxygenated-induced conductance, absent from normal RBCs, which shares some of the properties of P(sickle): equivalent Na(+) and K(+) permeability, significant Ca(2+) conductance, partial inhibition by DIDS and also Zn(2+). Gd(3+) markedly attenuates conductance in both normal and sickle RBCs. In addition, deoxygenated sickle cells, but not oxygenated ones or normal RBCs regardless of the oxygen tension, undergo haemolysis in isosmotic non-electrolyte solutions. Non-electrolyte entry was confirmed radioisotopically whilst haemolysis was inhibited by DIDS. These findings suggest that under certain circumstances P(sickle) may also be permeable to non-electrolytes. Finally, RBCs from certain patients with hereditary stomatocytosis have a mutated band 3, which appears able to act as a conductance pathway for univalent cations. These results extend our understanding of the abnormal permeability pathways of RBCs.

Authors+Show Affiliations

Department of Physiology, Anatomy and Genetics, Sherrington Building, Parks Road, Oxford, OX1 3PT, UK.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17434766

Citation

Ellory, J C., et al. "Abnormal Permeability Pathways in Human Red Blood Cells." Blood Cells, Molecules & Diseases, vol. 39, no. 1, 2007, pp. 1-6.
Ellory JC, Robinson HC, Browning JA, et al. Abnormal permeability pathways in human red blood cells. Blood Cells Mol Dis. 2007;39(1):1-6.
Ellory, J. C., Robinson, H. C., Browning, J. A., Stewart, G. W., Gehl, K. A., & Gibson, J. S. (2007). Abnormal permeability pathways in human red blood cells. Blood Cells, Molecules & Diseases, 39(1), 1-6.
Ellory JC, et al. Abnormal Permeability Pathways in Human Red Blood Cells. Blood Cells Mol Dis. 2007 Jul-Aug;39(1):1-6. PubMed PMID: 17434766.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Abnormal permeability pathways in human red blood cells. AU - Ellory,J C, AU - Robinson,H C, AU - Browning,J A, AU - Stewart,G W, AU - Gehl,K A, AU - Gibson,J S, Y1 - 2007/04/16/ PY - 2007/02/16/received PY - 2007/02/19/accepted PY - 2007/4/17/pubmed PY - 2007/9/27/medline PY - 2007/4/17/entrez SP - 1 EP - 6 JF - Blood cells, molecules & diseases JO - Blood Cells Mol Dis VL - 39 IS - 1 N2 - A number of situations that result in abnormal permeability pathways in human red blood cells (RBCs) have been investigated. In sickle cell disease (SCD), RBCs contain HbS, rather than the normal HbA. When deoxygenated, an abnormal conductance pathway, termed P(sickle), is activated, which contributes to cell dehydration, largely through allowing Ca(2+) entry and subsequent activation of the Gardos channel. Whole-cell patch-clamp recordings from sickle RBCs show a deoxygenated-induced conductance, absent from normal RBCs, which shares some of the properties of P(sickle): equivalent Na(+) and K(+) permeability, significant Ca(2+) conductance, partial inhibition by DIDS and also Zn(2+). Gd(3+) markedly attenuates conductance in both normal and sickle RBCs. In addition, deoxygenated sickle cells, but not oxygenated ones or normal RBCs regardless of the oxygen tension, undergo haemolysis in isosmotic non-electrolyte solutions. Non-electrolyte entry was confirmed radioisotopically whilst haemolysis was inhibited by DIDS. These findings suggest that under certain circumstances P(sickle) may also be permeable to non-electrolytes. Finally, RBCs from certain patients with hereditary stomatocytosis have a mutated band 3, which appears able to act as a conductance pathway for univalent cations. These results extend our understanding of the abnormal permeability pathways of RBCs. SN - 1079-9796 UR - https://www.unboundmedicine.com/medline/citation/17434766/Abnormal_permeability_pathways_in_human_red_blood_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1079-9796(07)00038-1 DB - PRIME DP - Unbound Medicine ER -