Patch-Clamp Analysis of Membrane Transport in Erythrocytes

Bouyer, Guillaume; Thomas, Serge; Egée, Stéphane

doi:10.5772/37279

Cited by 9 publications

(8 citation statements)

References 144 publications

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“… schematic overview of RBC ion pumps ( Sachs, 2003 ; Tiffert et al, 2003 ), symporters and antiporters ( Bernhardt et al, 1988 ; Wolfersberger, 1994 ) and ion channels ( Bouyer et al, 2012 ; Kaestner, 2011 , 2015 ). …”

Section: Determinants Of Rbc Deformabilitymentioning

confidence: 99%

Squeezing for Life – Properties of Red Blood Cell Deformability

et al. 2018

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Deformability is an essential feature of blood cells (RBCs) that enables them to travel through even the smallest capillaries of the human body. Deformability is a function of (i) structural elements of cytoskeletal proteins, (ii) processes controlling intracellular ion and water handling and (iii) membrane surface-to-volume ratio. All these factors may be altered in various forms of hereditary hemolytic anemia, such as sickle cell disease, thalassemia, hereditary spherocytosis and hereditary xerocytosis. Although mutations are known as the primary causes of these congenital anemias, little is known about the resulting secondary processes that affect RBC deformability (such as secondary changes in RBC hydration, membrane protein phosphorylation, and RBC vesiculation). These secondary processes could, however, play an important role in the premature removal of the aberrant RBCs by the spleen. Altered RBC deformability could contribute to disease pathophysiology in various disorders of the RBC. Here we review the current knowledge on RBC deformability in different forms of hereditary hemolytic anemia and describe secondary mechanisms involved in RBC deformability.

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Section: Determinants Of Rbc Deformabilitymentioning

confidence: 99%

Squeezing for Life – Properties of Red Blood Cell Deformability

et al. 2018

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“…Such consistency can be shown for a number of channels; just to name successful examples, the voltage-dependent anion channel (VDAC) (Bouyer et al, 2011 , 2012 ) and the NMDA-receptor (Makhro et al, 2013 ; Hänggi et al, 2014 ). However, providing a general correlation between patch-clamp and molecular biology derived results has had limited success (Kaestner, 2011 ; Bouyer et al, 2012 ). One reason for this difficulty is that techniques themselves or their particular application have certain shortcomings.…”

mentioning

confidence: 92%

Channelizing the red blood cell: molecular biology competes with patch-clamp

Kaestner

2015

Front. Mol. Biosci.

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“…Later, in addition to the K + (Na + )/H + exchanger (Richter et al, 1997 ; Kummerow et al, 2000 ), the existence of a voltage-activated non-selective cation channel was functionally demonstrated utilizing the patch-clamp technique (Christophersen and Bennekou, 1991 ; Kaestner et al, 1999 ; Rodighiero et al, 2004 ). At present, the molecular identity of this particular channel remains unknown (Kaestner, 2011 ; Bouyer et al, 2012 ), and it has alternatively been proposed to reflect a conductance state of the voltage-dependent anion channel (VDAC) (Bouyer et al, 2011 ). On the other hand, evidence for the existence of a number of voltage-activated Ca 2+ channels that are abundant in RBCs has been reported (Pinet et al, 2002 ; Romero et al, 2006 ), and the most convincing evidence is for Ca V 2.1, based on molecular biology data (Western blot) (Andrews et al, 2002 ) and, presumably, Ca V 2.1-specific pharmacological interactions (ω-agatoxinTK) (Andrews et al, 2002 ; Wagner-Britz et al, 2013 ).…”

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confidence: 99%