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1

Newer facets of sickle cell adhesiveness

100%
Shohet S. B., Thevenin B. J. M., Sherman I. W., Andrian U.
Cellular and Molecular Biology Letters
|
1998
|
tom 03
|
nr 4
To further explore the finding that peptides derived from specifically exposed regions of band 3 inhibited sickle cell adhesiveness in vitro, we examined the effects of such peptides with human sickle cells in the mouse microcirculation in vivo. Human red cells were loaded with the fluorescent dye BCECF, and infused into the arterial circulation of anaesthetized mice. The microcirculation of several tissues was examined in a specially designed warm-stage microscope with stroboscopic epi-fluorescent illumination. Adhesive events were video-recorded and quantified after peptide infusion and after treatment of the mice with various biological modifiers. An adhesive index (AI), proportionate to the number of adhesive events per number of cells entering a vessel, was calculated. Sickle cells (SS) were found to be more adhesive than normal cells particularly in small vessels such as post-capillary venules of the cremaster muscle (AI 2.3 vs 0.5). Moreover, endothelium activation substantially increased SS adhesiveness (e.g., AI 8.3 after pretreatment with platelet activating factor (PAF), 5.8 with tumor necrosis factor, and 8.7 with thrombin-activated mouse platelets). A band 3 peptide which blocked SS adhesiveness in vitro inhibited much of the increased adhesiveness of SS cells (e.g., in the PAF-treated mouse AI 2.8 vs 8.3, vs pretreatment control 2.3). No inhibitory effect was seen with a control peptide with the same composition but a scrambled sequence. These preliminary findings suggest that the inhibitory activity of specific band 3 sequences on SS adhesiveness is retained in vivo and extend the previous in vitro demonstration of an adhesive role for these exposed band 3 sequences. In addition, they imply a substantial role for endothelial and/or platelet activation in the adhesiveness of sickle cells in vivo. Finally, they demonstrate the utility of direct visualization of the mouse microcirculation for studying the adhesiveness of human cells.
2

Newer facets of sickle cell adhesiveness

100%
Shohet S. B., Thevenin B. J. M.
Cellular and Molecular Biology Letters
|
1998
|
tom 03
|
nr 2
3

Protein profiling of sickle cell versus control RBC core membrane skeletons by ICAT technology and tandem mass spectrometry

100%
Chou J., Choudhary P. K., Goodman S. R.
Cellular and Molecular Biology Letters
|
2006
|
tom 11
|
nr 3
A proteomic approach using a cleavable ICAT reagent and nano-LC ESI tandem mass spectrometry was used to perform protein profiling of core RBC membrane skeleton proteins between sickle cell patients (SS) and controls (AA), and determine the efficacy of this technology. The data was validated through Peptide/Protein Prophet and protein ratios were calculated through ASAPratio. Through an ANOVA test, it was determined that there is no significant difference in the mean ratios from control populations (AA1/AA2) and sickle cell versus control populations (AA/SS). The mean ratios were not significantly different from 1.0 in either comparison for the core skeleton proteins (α spectrin, β spectrin, band 4.1 and actin). On the natural-log scale, the variation (standard deviation) of the method was determined to be 14.1% and the variation contributed by the samples was 13.8% which together give a total variation of 19.7% in the ratios.
4

Erythrocyte spectrin is an E2 ubiquitin conjugating enzyme

100%
Goodman S. R., Kakhniashvili D. G., Sangerman J., Chaudhary T., Zimmer W. E., Bencsath F. A., Jardine I.
Cellular and Molecular Biology Letters
|
2001
|
tom 06
|
nr 2
5

The spectrin membrane skeleton: a key element in sickle cell disease

100%
Goodman S. R.
Cellular and Molecular Biology Letters
|
1998
|
tom 03
|
nr 2
6

The role of the membrane skeleton in formation of the irreversibly sickled cell: a review

84%
Goodman S. R.
Cellular and Molecular Biology Letters
|
1996
|
tom 01
|
nr 1
In this review we discuss the evidence in support of the concept that a posttranslational modification in β-actin, in which a disulfide bridge is formed between cysteine284 and cysteine373, is the major cause of the formation of the irreversibly sickled cell (ISC). This ISC β-actin modification caused a decreased ability of the ISC membrane skeletal proteins to disassemble, as compared to the control and reversible sickled cell (RSC) membrane skeleton, because of altered actin filament formation. The slow disassembly of the ISC membrane skeleton proteins gives a reasonable explanation for the inability of the ISC to remodel its shape. An understanding of the molecular basis of the irreversibly sickled cells formation has helped initiate a rationale for development of drugs to block ISC formation in vivo.
7

Modulated human globin gene expression: role for antisense expression vectors

84%
Xu L., Pace B. S.
Cellular and Molecular Biology Letters
|
1998
|
tom 03
|
nr 4
Several approaches have been explored to prevent polymerization of sickle hemoglobin in erythrocytes. We tested the ability of a mammalian expression vector carrying a β gene antisense cDNA fragment to block β gene expression. The antisense expression vector was stably transfected into HS2γβ stable mouse erythroleukemia cell lines producing human γ and β globin chains. By day 14 there was an average 24% decrease and 12% increase in β and γ globin mRNA levels respectively. We observed a loss of β gene inhibition by day 42. This study suggests that a β globin antisense cDNA expression vector may be an alternative gene therapy strategy to decrease sickle hemoglobin levels in patient with sickle cell disease.
8

New therapeutic approaches to sickle cell disease: targeting RBC membrane oxidative damage

67%
Goodman S. R., Pace B. S., Shartava A.
Cellular and Molecular Biology Letters
|
1998
|
tom 03
|
nr 4
In this brief review, we discuss evidence leading to the conclusion that diminished levels of reduced glutathione combined with increased oxygen radical production leads to oxidative damage to membrane proteins in sickle cell disease erythrocytes. Among these oxidatively damaged proteins are K+-channels (Gardos channel and K+-Cl--channel) and β-actin. Oxidative damage to the K+-channels leads to K+ leakage and H2O loss from light density reversibly sickled cells (RSCs). The resulting dense RSCs are primarily sickled in shape due to increased [HbS] and increased polymerization. The oxidation of β-actin converts the dense RSCs to dense irreversibly sickled cells (ISCs) as explained in our two step model. Furthermore, we discuss recent in vitro evidence that N-acetylcysteine (NAC) can block the formation of dense cells and ISCs by protecting the K+-channels and β-actin respectively from oxidative damage. Finally we describe an ongoing Phase II human trial to determine whether NAC can also lower dense cells and ISCs in vivo and, if so, result in fewer painful vasooclusive episodes.
9

Plasma membrane phospholipid asymmetry and its maintenance

51%
Roelofsen B., Vermeulen W. P., Op den Kamp J.A.F.
Biophysics of Membrane Transport
|
1994
|
tom 12
|
nr 2
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