1,721,216 research outputs found
Letter to the editor regarding the article by Chen et al. entitled “Protective effects of echinacoside against anoxia/reperfusion injury in H9c2 cells via up-regulating p-AKT and SLC8A3”
Full text linkThe dual face of glutamate: from a neurotoxin to a potential survival factor—metabolic implications in health and disease
Full text linkGlutamate is the major excitatory neurotransmitter in the central nervous system. Beyond this function, glutamate also plays
a key role in intermediary metabolism in all organs and tissues, linking carbohydrate and amino acid metabolism via the
tricarboxylic acid cycle. Under both physiological and pathological conditions, we have recently found that the ability of
glutamate to fuel cell metabolism selectively relies on the activity of two main transporters: the sodium–calcium exchanger
(NCX) and the sodium-dependent excitatory amino-acid transporters (EAATs). In ischemic settings, when glutamate is
administered at the onset of the reoxygenation phase, the coordinate activity of EAAT and NCX allows glutamate to improve
cell viability by stimulating ATP production. So far, this phenomenon has been observed in both cardiac and neuronal models.
In this review, we focus on the most recent findings exploring the unusual activity of glutamate as a potential survival
factor in different settings
Calcium- and ATP-dependent regulation of Na/Ca exchange function in BHK cells: Comparison of NCX1 and NCX3 exchangers
No full textNa+/Ca2+ exchangers (NCX) mediate bidirectional Ca2+ fluxes across cell membranes and contribute to Ca2+ homeostasis in many cell types. Exchangers are regulated by gating reactions that depend on Na+ and Ca2+ binding to transport and regulatory sites. A Na+i-dependent inactivation is prominent in all isoforms, whereas Ca2+i-dependent regulation varies among isoforms. Here we characterize new details of NCX operation and describe differences and similarities between NCX3 and NCX1 regulation by intracellular Ca2+ and ATP. To compare isoforms, we employed BHK cells expressing NCX3 or NCX1 constitutively and exchange activity was analysed in whole-cell and excised patch recordings under "zero-trans" conditions (i.e., with only one transported ion species on each side). Using BHK cells with low cytoplasmic Ca2+ buffering, outward (reverse) currents, reflecting Ca2+ influx, are activated by applying extracellular Ca2+ (Cao) in the presence of Na+ on the cytoplasmic side. When firstly activated, peak outward NCX3 currents rapidly decay over seconds and then typically develop a secondary transient peak with slower kinetics, until Cao removal abolishes all outward current. The delayed rise of outward current is the signature of an activating process since peak outward NCX3 currents elicited at subsequent Cao bouts remain stimulated for minutes and slower decline towards a non-zero level during continued Cao application. Secondary transient peaks and current stimulation are suppressed by increasing the intracellular Ca2+ buffer capacity or by replacing cytoplasmic ATP with the analogues AMP-PNP or ATPγS. In BHK cells expressing NCX1, outward currents activated under identical settings decay to a steady-state level during single Cao application and are significantly larger, causing strong and long-lived run down of subsequent outward currents. NCX1 current run down is not prevented by increasing cytoplasmic Ca2+ buffering but secondary transient peaks in the outward current profile can be resolved in the presence of ATP. Finally, inward currents recorded in patches excised from NCX3-expressing cells reveal a proteolysis-sensitive, Ca-dependent inactivation process that is unusual for NCX1 forward activity. Together, our results suggest that NCX function is regulated more richly than appreciated heretofore, possibly including processes that are lost in excised membrane patches
The inhibition of the Na+-Ca++ exchanger enhances anoxia and glucopenia-induced (3H) aspartate release in hippocampal slices.
No full textCracking the code of sodium/calcium exchanger (NCX) gating: old and new complexities surfacing from the deep web of secondary regulations
No full textCell membranes spatially define gradients that drive the complexity of biological signals. To guarantee movements and exchanges of solutes between compartments, membrane transporters negotiate the passages of ions and other important molecules through lipid bilayers. The Na+/Ca2+ exchangers (NCXs) in particular play central roles in balancing Na+ and Ca2+ fluxes across diverse proteolipid borders in all eukaryotic cells, influencing cellular functions and fate by multiple means. To prevent progression from balance to disease, redundant regulatory mechanisms cooperate at multiple levels (transcriptional, translational, and post-translational) and guarantee that the activities of NCXs are finely-tuned to cell homeostatic requirements. When this regulatory network is disturbed by pathological forces, cells may approach the end of life. In this review, we will discuss the main findings, controversies and open questions about regulatory mechanisms that control NCX functions in health and disease
K+ channel openers activate brain sulfonylurea-sensitive K+ channels and block neurosecretion
No full textImmunocytochemical localization of calretinin-containing neurons in the rat periaqueductal gray and colocalization with enzymes producing Nitric Oxide: a double, double-labeling study
No full textDoping engineering for random telegraph noise suppression in deca-nanometer Flash memories
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