In vitro effects of thyroxine on the mechanical properties of erythrocytes

Başkurt, O.K.; Levi, Edi; Temizer, A.; Ozer, Duri; Caglayan, Serdar; Dikmenoglu, Neslihan; Andaç, S.O.

doi:10.1016/0024-3205(90)90464-3

Cited by 15 publications

(11 citation statements)

References 12 publications

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“…The action of thyroid hormone on plasma membrane Ca2+-ATPase activity requires the presence of the calmodulin Ca2+ complex (43). In human red cells, we have confirmed that this stimulation of Ca2+-ATPase activity by l-T4 and L-T3 is associated with increased 45Ca2+ efflux (44) and others have shown that human red cell Ca2+ content decreases when intact erythrocytes are incubated in vitro with physiologically relevant concentrations of T4 (45). Red cells from patients with end-stage renal disease (ESRD) have increased Ca2+ content (46) and decreased Ca2+-ATPase activity (46,47) and 45Ca2+ efflux from ESRD red cells is unresponsive to T4 and T3 (47).…”

Section: Actions Of Thyroid Hormone At the Plasma Membranesupporting

confidence: 77%

Nongenomic Actions of Thyroid Hormone

Davis

Davis²

1996

Thyroid

247

106

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Nongenomic actions of thyroid hormone are by definition independent of nuclear receptors for the hormone and have been described at the plasma membrane, various cell organelles, the cytoskeleton, and in cytoplasm. The actions include alterations in solute transport (Ca2+, Na+, glucose), changes in activities of several kinases, including protein kinase C, cAMP-dependent protein kinase and pyruvate kinase M2 (PKM2), effects on efficiency of specific mRNA translation and mRNA t1/2, modulation of mitochondrial respiration, and regulation of actin polymerization (promotion of formation of F-actin). Iodothyronines also can regulate nongenomically the state of contractile elements in vascular smooth muscle cells (VSMC). The physiologic significance at the cellular level of certain of these actions has been demonstrated, for example, in the cases of myocardiocyte Na+ current, red cell Ca2+ content, and the control by hormone-induced alterations in actin solubility of cell surface activity of iodothyronine 5'-monodeiodinase activity and the intracellular distribution of protein disulfide isomerase activity. The physiologic significance of these actions at the organ or system level is less clear, but extranuclear effects of thyroid hormone on myocardial Na+ channel, sarcoplasmic reticulum Ca(2+)-ATPase activity, and contractile state of VSMC may each contribute to acute effects of thyroid hormone on cardiac output that have recently been described clinically. The molecular mechanisms for nongenomic actions are incompletely understood; relevant binding sites and signal transduction pathways have been described for hormone actions on plasma membrane Ca(2+)-ATPase activity, and PKM2 monomer is known to bind T3 and, as a result, prevent activation of the kinase via tetramer formation. Nongenomic actions of thyroid hormone may have different structure-activity relationships of iodothyronines from those effects that depend upon nuclear receptors; they may have different time courses and may invoke complex signal transduction pathways before the action is detected.

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Section: Actions Of Thyroid Hormone At the Plasma Membranesupporting

confidence: 77%

Nongenomic Actions of Thyroid Hormone

Davis

Davis²

1996

Thyroid

247

106

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“…It thus seems reasonable to assume that our ektacytometer findings indicate RBC equilibrium deformation at a given SS for any time point beyond ∼0.2 s. Further, the very significant differences in the time constants measured in the suspensions with different calcium contents under the same SS (Fig. 6) also support the notion that EI-time relations reflect cellular behavior, as calcium levels affect RBC mechanical properties [5,18,32] yet do not alter the fluid mechanics of the system. The mechanisms involved in the observed improvement in EI have not been fully detailed in the present study.…”

Section: Discussionsupporting

confidence: 64%

“…Mechano-sensitive calcium channels have been shown to exist in the RBC membrane [10] and to respond to local deformations of the membrane to increase calcium permeability [15]. Intracellular calcium concentration has long been considered an important determinant of RBC deformability [5,18,32]. Further, extracellular calcium is a determinant of RBC sub-hemolytic damage under extremely high SS [35], although this finding could not be confirmed in experiments utilizing lower SS [9].…”

Section: Discussionmentioning

confidence: 99%

Shear stress-induced improvement of red blood cell deformability

et al. 2013

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Classically, it is known that red blood cell (RBC) deformability is determined by the geometric and material properties of these cells. Experimental evidence accumulated during the last decade has introduced the concept of active regulation of RBC deformability. This regulation is mainly related to altered associations between membrane skeletal proteins and integral proteins, with the latter serving to anchor the skeleton to the lipid matrix. It has been hypothesized that shear stress induces alterations of RBC deformability: the current study investigated the dynamics of the transient improvement in deformability induced by shear stress at physiologically-relevant levels. RBC were exposed to various levels of shear stress (SS) in a Couette type shearing system that is part of an ektacytometer, thus permitting the changes in RBC deformability during the application of SS to be monitored. Initial studies showed that there is an increase in deformability of the RBC subjected to SS in the range of 5-20 Pa, with kinetics characterized by time constants of a few seconds. Such improvement in deformability, expressed by an elongation index (EI), was faster with higher levels of SS and hence yielded shorter time constants: absolute values of EI increased by 3-8% of the starting level. Upon the removal of the shear stress, this response by RBC was reversible with a slower time course compared to the increase in EI during application of SS. Increased calcium concentration in the RBC suspending medium prevented the improvement of deformability. It is suggested that the improvement of RBC deformability by shear forces may have significant effects on blood flow dynamics, at least in tissues supplied by blood vessels with impaired vasomotor reserve, and may therefore serve as a compensating mechanism for the maintenance of adequate microcirculatory perfusion.

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“…RBC have unique mechanical properties which determine their behavior under flow conditions. Deformability refers to the shape change under external forces , which is fully reversible upon the removal of the deforming forces, the shape recovery having time constants in the order of 0.1 second . RBC deformability is the key property behind the significantly reduced blood viscosity at high flow rates as well as in the microcirculatory blood flow .…”

Section: Red Blood Cell Functionsmentioning

confidence: 99%

Tissue Oxygen Demand in Regulation of the Behavior of the Cells in the Vasculature

et al. 2013

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The control of arteriolar diameters in microvasculature has been in the focus of studies on mechanisms matching oxygen demand and supply at the tissue level. Functionally, important vascular elements include EC, VSMC, and RBC. Integration of these different cell types into functional units aimed at matching tissue oxygen supply with tissue oxygen demand is only achieved when all these cells can respond to the signals of tissue oxygen demand. Many vasoactive agents that serve as signals of tissue oxygen demand have their receptors on all these types of cells (VSMC, EC, and RBC) implying that there can be a coordinated regulation of their behavior by the tissue oxygen demand. Such functions of RBC as oxygen carrying by Hb, rheology, and release of vasoactive agents are considered. Several common extra- and intracellular signaling pathways that link tissue oxygen demand with control of VSMC contractility, EC permeability, and RBC functioning are discussed.

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In vitro effects of thyroxine on the mechanical properties of erythrocytes

Cited by 15 publications

References 12 publications

Nongenomic Actions of Thyroid Hormone

Nongenomic Actions of Thyroid Hormone

Shear stress-induced improvement of red blood cell deformability

Tissue Oxygen Demand in Regulation of the Behavior of the Cells in the Vasculature

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