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Intracellular Na+ (intracellular + na+)

Distribution by Scientific Domains

Medical Sciences	66%
Life Sciences	33%

Terms modified by Intracellular Na+

intracellular na+ concentration

Selected Abstracts

Intracellular Na+ and Ca2+ modulation increases the tensile properties of developing engineered articular cartilage

ARTHRITIS & RHEUMATISM, Issue 4 2010
Roman M. Natoli
Objective Significant collagen content and tensile properties are difficult to achieve in tissue-engineered articular cartilage. The aim of this study was to investigate whether treating developing tissue-engineered cartilage constructs with modulators of intracellular Na+ or Ca2+ could increase collagen concentration and construct tensile properties. Methods Inhibitors of Na+ ion transporters and stimulators of intracellular Ca2+ were investigated for their ability to affect articular cartilage development in a scaffoldless, 3-dimensional chondrocyte culture. Using a systematic approach, we applied ouabain (Na+/K+ -ATPase inhibitor), bumetanide (Na+/K+/2Cl, tritransporter inhibitor), histamine (cAMP activator), and ionomycin (a Ca2+ ionophore) to tissue-engineered constructs for 1 hour daily on days 10,14 of culture and examined the constructs at 2 weeks or 4 weeks. The gross morphology, biochemical content, and compressive and tensile mechanical properties of the constructs were assayed. Results The results of these experiments showed that 20 ,M ouabain, 0.3 ,M ionomycin, or their combination increased the tensile modulus by 40,95% compared with untreated controls and resulted in an increased amount of collagen normalized to construct wet weight. In constructs exposed to ouabain, the increased percentage of collagen per construct wet weight was secondary to decreased glycosaminoglycan production on a per-cell basis. Treatment with 20 ,M ouabain also increased the ultimate tensile strength of neo-tissue by 56,86% at 4 weeks. Other construct properties, such as construct growth and type I collagen production, were affected differently by Na+ modulation with ouabain versus Ca2+ modulation with ionomycin. Conclusion These data are the first to show that treatments known to alter intracellular ion concentrations are a viable method for increasing the mechanical properties of engineered articular cartilage and identifying potentially important relationships to hydrostatic pressure mechanotransduction. Ouabain and ionomycin may be useful pharmacologic agents for increasing tensile integrity and directing construct maturation. [source]

The death of cardiotonic steroid-treated cells: evidence of Na+i,K+i -independent H+i -sensitive signalling

ACTA PHYSIOLOGICA, Issue 1-2 2006
S. N. Orlov
Abstract Na/K-ATPase is the only known target of cardiotonic steroids (CTS) identified in plants, amphibians and later on in several mammalian species, including human. We focus our review on recent data implicating CTS in the tissue-specific regulation of cell survival and death. In vascular smooth muscle cells, CTS inhibited cell death triggered by apoptotic stimuli via a novel Na+i -mediated, Ca2+i -independent mechanism of expression of antiapoptotic genes, including mortalin. In contrast, exposure to CTS in vascular endothelial and renal epithelial cells led to cell death, showing combined markers of apoptosis and necrosis. This mode of cell death, termed oncosis, is caused by CTS interaction with Na/K-ATPase but is independent of the inhibition of Na/K-ATPase-mediated ion fluxes and inversion of the [Na+]i/[K+]i ratio. The intermediates of intracellular signalling involved in Na+i, K+i -independent oncosis of CTS-treated cells remain unknown. Recently, we found that this mode of cell death can be protected by modest intracellular acidification via the expression of H+i -sensitive genes. The molecular origin of intracellular Na+ and H+ sensor involvement in the development of apoptosis and oncosis is currently under investigation. [source]

Changes in intracellular Na+ in heart failure following SERCA knockout , more of a solution or more of a problem?

THE JOURNAL OF PHYSIOLOGY, Issue 7 2010
J. Andrew Wasserstrom
No abstract is available for this article. [source]

Intracellular Na+ and Ca2+ modulation increases the tensile properties of developing engineered articular cartilage

Four new cases of stomatin-deficient hereditary stomatocytosis syndrome: association of the stomatin-deficient cryohydrocytosis variant with neurological dysfunction

BRITISH JOURNAL OF HAEMATOLOGY, Issue 6 2004
Britta Fricke
Summary This report concerns congenitally Na+,K+ leaky red cells of the ,hereditary stomatocytosis' class. Three new isolated cases and one new pedigree are described, and one previously reported case is expanded. In all cases, Western blotting of red cell membranes revealed a deficiency in the 32 kDa membrane protein, stomatin. All showed pronounced cation leaks at 37°C with markedly abnormal intracellular Na+ and K+ concentrations, like all other such stomatin-deficient cases. Consistent with recent findings in two previously described British pedigrees, immunocytochemistry demonstrated that the deficiency of stomatin was not complete. On typical blood films, some red cells showed positive stomatin immunoreactivity, while most were negative, although in one case only a minority were negative. All platelets and neutrophils were stomatin positive. The cases differed markedly between themselves with regard to the temperature dependence of the passive leak to K+. Three showed a simple monotonic temperature dependence, while two showed a minimum at around 20,25°C, such that the cells were extremely leaky at 0°C, giving the phenotype known as ,cryohydrocytosis'. These patients are the only two known cases of stomatin-deficient cryohydrocytosis. Both showed a congenital syndrome of mental retardation, seizures, cataracts and massive hepatosplenomegaly, probably defining a new haemato-neurological syndrome. [source]

Four pedigrees of the cation-leaky hereditary stomatocytosis class presenting with pseudohyperkalaemia.

BRITISH JOURNAL OF HAEMATOLOGY, Issue 4 2004
K+ leak in a xerocytic form, Novel profile of temperature dependence of Na+
Summary We report four pedigrees of the group of Na+,K+ -leaky red cell disorders of the ,hereditary stomatocytosis' class. Each showed pseudohyperkalaemia because of temperature-dependent loss of K+ from red cells on storage of whole blood at room temperature. All pedigrees showed an abnormality in the temperature dependence of the ,passive leak' of the membrane to K+. Two pedigrees, both of which showed a compensated haemolytic state with dehydrated red cells and target cells on the blood film, showed a novel pattern, in which the profile was flat between 37°C and about 32°C then dropped as the temperature was reduced to zero. The third showed the ,shallow slope' profile, with stomatocytes on the blood film and very markedly abnormal intracellular Na+ and K+ levels. Minimal haemolysis was present. The fourth pedigree, of Asian origin, showed the shoulder pattern (minimum at 32°C, maximum at 12°C) with essentially normal haematology. Both of these latter two forms have previously been seen in other pedigrees. The first variant represents a novel kind of temperature dependence of the passive leak found in these pedigrees presenting with pseudohyperkalaemia. [source]