Red cell surface structure: Stabilization by cholesterol sulfate as evidenced by scanning electron microscopy

Bleau, G.; Lalumière, Gaston; Chapdelaine, A.; Roberts, Kenneth D.

doi:10.1016/0005-2736(75)90190-x

Cited by 45 publications

(12 citation statements)

References 3 publications

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“…This idea was supported by the finding that cholesterol sulfate at physiologic concentrations protected red blood cells against osmotic lysis, an effect requiring both the sulfate moiety and the cholesterol side chain (54,92). This novel finding, along with the knowledge that cholesterol sulfate is widely distributed among human tissues, led to the hypothesis that cholesterol sulfate might be an important constituent of many types of biological membranes where it can function as a stabilizing agent (54).…”

Section: Membranesmentioning

confidence: 92%

Cholesterol sulfate in human physiology: what's it all about?

Strott

Higashi

2003

Journal of Lipid Research

196

184

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Cholesterol sulfate is quantitatively the most important known sterol sulfate in human plasma, where it is present in a concentration that overlaps that of the other abundant circulating steroid sulfate, dehydroepiandrosterone (DHEA) sulfate. Although these sulfolipids have similar production and metabolic clearance rates, they arise from distinct sources and are metabolized by different pathways. While the function of DHEA sulfate remains an enigma, cholesterol sulfate has emerged as an important regulatory molecule. Cholesterol sulfate is a component of cell membranes where it has a stabilizing role, e.g., protecting erythrocytes from osmotic lysis and regulating sperm capacitation. It is present in platelet membranes where it supports platelet adhesion. Cholesterol sulfate can regulate the activity of serine proteases, e.g., those involved in blood clotting, fibrinolysis, and epidermal cell adhesion. As a result of its ability to regulate the activity of selective protein kinase C isoforms and modulate the specificity of phosphatidylinositol 3-kinase, cholesterol sulfate is involved in signal transduction. Cholesterol sulfate functions in keratinocyte differentiation, inducing genes that encode for key components involved in development of the barrier. The accumulating evidence demonstrating a regulatory function for cholesterol sulfate appears solid; the challenge now is to work out the molecular mechanisms whereby this interesting molecule carries out its various roles. -Strott, C. A., and Y. Higashi. Cholesterol sulfate in human physiology: what's it all about? J.

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Section: Membranesmentioning

confidence: 92%

Cholesterol sulfate in human physiology: what's it all about?

Strott

Higashi

2003

Journal of Lipid Research

196

184

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“…Ch-S was shown to protect the human RBC against hypotonic hemolysis. At physiological concentrations of Ch-S, the sulfate moiety, as well as the side chain of Ch-S, were both shown to be necessary to biological activity in vitro [271]. Figure 6 shows a graphical depiction of cholesterol sulfate in the red blood cell membrane, and Figures 7 and 8 show how the shapes of red blood cells change under the influence of Ch-S. M cholesterol sulfate.…”

Section: The Role Of Bio-sulfates In Maintaining Cell Membrane Functionmentioning

confidence: 99%

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Davidson¹,

Seneff²

2012

Entropy

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Abstract:In reviewing the literature pertaining to interfacial water, colloidal stability, and cell membrane function, we are led to propose that a cascade of events that begins with acute exogenous surfactant-induced interfacial water stress can explain the etiology of sudden death syndrome (SDS), as well as many other diseases associated with modern times. A systemic lowering of serum zeta potential mediated by exogenous cationic surfactant administration is the common underlying pathophysiology. The cascade leads to subsequent inflammation, serum sickness, thrombohemorrhagic phenomena, colloidal instability, and ultimately even death. We propose that a sufficient precondition for sudden death is lowered bioavailability of certain endogenous sterol sulfates, sulfated glycolipids, and sulfated glycosaminoglycans, which are essential in maintaining biological equipose, energy metabolism, membrane function, and thermodynamic stability in living organisms. Our literature review provides the basis for the presentation of a novel hypothesis as to the origin of endogenous bio-sulfates which involves energy transduction from sunlight. Our hypothesis is amply supported by a growing body of data showing that parenteral administration of substances that lower serum zeta potential results in kosmotropic cationic and/or chaotropic anionic interfacial water stress, and the resulting cascade.Keywords: inflammation; serum sickness; colloidal instability; interfacial water stress; bio-sulfates; Shwartzman phenomena; sudden death syndrome Glossary of TermsAnaphylaxis a severe, rapidly progressing, life-threatening, generalized allergic reaction. Biological equipoise a stable, non-equilibrium, dissipative system synonymous with life. Cholesterol sulfate (Ch-S)quantitatively the most important known sterol sulfate in human plasma where it regulates the activity of the serine proteases, in cell membranes where it has a stabilizing role, and in platelet membranes where it supports platelet adhesion. Coherence domain (CD)a water CD is a collection of liquid water molecules which oscillate in unison in tune with a self-trapped electromagnetic field at a well-defined frequency. The coherent oscillations produce an ensemble of quasi-free electrons, able to collect noise energy from the environment and transform it into high-grade coherent energy in the form of electron vortices. This high-grade energy may then activate biomolecules resonating with the water CD. Colloidal instabilitya property attributed to a colloidal suspension that develops when stabilizing repulsive steric and electrostatic forces between colliding particles are insufficient to prevent their natural tendency to aggregate into masses large enough to precipitate.Colloidal suspension a colloid that has a continuous liquid phase in which a solid is suspended in a liquid, e.g., our flowing blood. Exclusion zone (EZ)a glass-like, gel phase consisting of water CDs resonating in-phase, adjacent to hydrophilic surfaces, several hundred micrometers wide which excludes colloi...

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“…11,12 Interestingly, cholesterol sulfate has emerged as a multifaceted regulatory molecule. 13 Its presence in cell membranes protects erythrocytes against osmotic lysis 10,14 and regulates sperm capacitation. 15,16 In platelets, cholesterol sulfate has been shown to support platelet adhesion.…”

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confidence: 99%

Expression of Cholesterol Sulfotransferase (SULT2B1b) in Human Platelets

et al. 2004

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Background-Cholesterol sulfate, the most important sterol sulfate in the human circulation, has emerged as a multifaceted molecule. Among its many demonstrated regulatory actions is its ability to influence blood clotting and fibrinolysis. Additionally, cholesterol sulfate is a constituent of human platelets, where it has been shown to support platelet aggregation. Methods and Results-We have documented the presence of the enzyme (SULT2B1b) that sulfonates cholesterol in human platelets and examined the influence of plasma lipoproteins on the expression and activity of this enzyme. SULT2B1b mRNA was detected by reverse transcription-polymerase chain reaction and found to be the only steroid/sterol sulfotransferase expressed in these discoid anucleate particles. Using real-time polymerase chain reaction for quantification, we found that the level of SULT2B1b mRNA in platelets was maintained at 4°C but substantially diminished over a period of 4 hours at 37°C. The loss of SULT2B1b mRNA, however, was markedly reduced in the presence of HDL but not LDL. The stabilizing influence of HDL was attributable specifically to its apolipoprotein (apo) A-I component, whereas apoA-II and apoE were without effect. Importantly, there was a direct correlation between platelet SULT2B1b mRNA and protein levels in the presence or absence of lipoprotein that was reflected in enzymatic activity and cholesterol sulfate production. Conclusions-Human platelets selectively express SULT2B1b, the physiological cholesterol sulfotransferase. Furthermore, the stability of SULT2B1b mRNA and protein in platelets maintained at 37°C is subject to regulation by the apoA-I component of HDL.

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Red cell surface structure: Stabilization by cholesterol sulfate as evidenced by scanning electron microscopy

Cited by 45 publications

References 3 publications

Cholesterol sulfate in human physiology: what's it all about?

Cholesterol sulfate in human physiology: what's it all about?

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Expression of Cholesterol Sulfotransferase (SULT2B1b) in Human Platelets

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