The Experts below are selected from a list of 10416 Experts worldwide ranked by ideXlab platform
Francisco Zafra - One of the best experts on this subject based on the ideXlab platform.
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activity dependent internalization of the glutamate transporter glt 1 requires calcium entry through the ncx sodium calcium Exchanger
Neurochemistry International, 2019Co-Authors: Ignacio Ibanez, David Bartolomemartin, Dolores Piniella, Cecilio Gimenez, Francisco ZafraAbstract:Abstract GLT-1 is the main glutamate transporter in the brain and its trafficking controls its availability at the cell surface, thereby shaping glutamatergic neurotransmission under physiological and pathological conditions. Extracellular glutamate is known to trigger ubiquitin-dependent GLT-1 internalization from the surface of the cell to the intracellular compartment, yet here we show that internalization also requires the participation of calcium ions. Consistent with previous studies, the addition of glutamate (1 mM) to mixed primary cultures (containing neurons and astrocytes) promotes GLT-1 internalization, an effect that was suppressed in the absence of extracellular Ca2+. The pathways of Ca2+ mobilization by astrocytes were analyzed in these mixed cultures using the genetically encoded calcium sensor GCaMP6f. A complex pattern of calcium entry was activated by glutamate, with a dramatic and rapid rise in the intracellular Ca2+ concentration partially driven by glutamate transporters, especially in the initial stages after exposure to glutamate. The Na+/Ca2+ Exchanger (NCX) plays a dominant role in this Ca2+ mobilization and its blockade suppresses the glutamate induced internalization of GLT-1, both in astrocytes and in a more straightforward experimental system like HEK293 cells transiently transfected with GLT-1. This regulatory mechanism might be relevant to control the amount of GLT-1 transporter at the cell surface in conditions like ischemia or traumatic brain injury, where extracellular concentrations of glutamate are persistently elevated and they promote rapid Ca2+ mobilization.
Changbaig Hyun - One of the best experts on this subject based on the ideXlab platform.
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the cardiac biomarker sodium calcium Exchanger ncx 1 can differentiate between heart failure and renal failure a comparative study of ncx 1 expression in dogs with chronic mitral valvular insufficiency and azotemia
Journal of Veterinary Internal Medicine, 2010Co-Authors: Changbaig HyunAbstract:Background: The Sodium-Calcium Exchanger (NCX-1), an established cardiac biomarker, was postulated previously as differentiating between heart failure (HF) and renal failure (RF) in dogs. The effect of azotemia on NCX-1 expression has not been studied. Hypothesis: In contrast to other cardiac biomarkers (eg, N-terminal-proBNP), we hypothesized that the expression level of NCX-1 is not influenced by either azotemia or decreased renal clearance. Animals: Fifteen client-owned healthy control dogs, 14 dogs with chronic mitral valvular insufficiency (CMVI), classified based on severity of the disease by the established International Small Animal Cardiac Health Council classification system, and 15 dogs with RF, grouped according to the International Renal Interest Society stage classification. Methods: A comparative study of the expression levels of NCX-1, evaluated in peripheral blood samples from dogs with HF, RF, and healthy controls by quantitative PCR. Results: NCX-1 expression was significantly increased in moderate (2.99 ± 0.61 [fold changes relative to normal group]) to severe (4.35 ± 1.44) CMVI dogs (P < .01). In contrast, NCX-1 expression was not increased in the azotemic dogs. Furthermore, there was also no correlation between increased concentrations of creatinine and urea nitrogen in serum and NCX-1 expression in the RF group. Conclusions and Clinical Importance: Azotemia likely does not affect NCX-1 expression.
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the cardiac sodium calcium Exchanger gene ncx 1 is a potential canine cardiac biomarker of chronic mitral valvular insufficiency
Journal of Veterinary Internal Medicine, 2008Co-Authors: Hyeongsun Moon, Eun Ju Choi, Changbaig HyunAbstract:Background: The cardiac Sodium-Calcium Exchanger gene (NCX-1) is upregulated in humans and mice with congestive heart failure (CHF). Hypothesis: NCX-1 expression is upregulated in dogs with heart failure from chronic mitral valvular insufficiency (CMVI). Animals: Client-owned 14 healthy control dogs and 30 dogs with CMVI. Methods: Prospective, controlled, observational study. We investigated the levels of NCX-1 expression in dogs at different stages of CMVI with real-time reverse transcription polymerase chain reaction. Results: The mRNA expression levels of NCX-1 were determined in peripheral blood samples obtained from the animals used in this study. Dogs were graded by the severity of disease. The fold differences in the levels of mRNA expression compared with controls were 1.39 ± 0.88 (group I), 1.32 ± 0.65 (group II), 4.86 ± 1.25 (group III), and 5.96 ± 1.69 (group IV). NCX-1 expression was significantly higher in groups III and IV (P < .05) compared with the healthy controls, whereas groups I and II were not. Conclusions and Clinical Importance: The level of NCX-1 expression was significantly higher in groups of dogs with moderate to severe CMVI (groups III and IV) compared with the controls. Our findings indicate that NCX-1 can be a biomarker for chronic valvular disease in dogs and is a potential biomarker for severity of heart disease.
Ignacio Ibanez - One of the best experts on this subject based on the ideXlab platform.
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activity dependent internalization of the glutamate transporter glt 1 requires calcium entry through the ncx sodium calcium Exchanger
Neurochemistry International, 2019Co-Authors: Ignacio Ibanez, David Bartolomemartin, Dolores Piniella, Cecilio Gimenez, Francisco ZafraAbstract:Abstract GLT-1 is the main glutamate transporter in the brain and its trafficking controls its availability at the cell surface, thereby shaping glutamatergic neurotransmission under physiological and pathological conditions. Extracellular glutamate is known to trigger ubiquitin-dependent GLT-1 internalization from the surface of the cell to the intracellular compartment, yet here we show that internalization also requires the participation of calcium ions. Consistent with previous studies, the addition of glutamate (1 mM) to mixed primary cultures (containing neurons and astrocytes) promotes GLT-1 internalization, an effect that was suppressed in the absence of extracellular Ca2+. The pathways of Ca2+ mobilization by astrocytes were analyzed in these mixed cultures using the genetically encoded calcium sensor GCaMP6f. A complex pattern of calcium entry was activated by glutamate, with a dramatic and rapid rise in the intracellular Ca2+ concentration partially driven by glutamate transporters, especially in the initial stages after exposure to glutamate. The Na+/Ca2+ Exchanger (NCX) plays a dominant role in this Ca2+ mobilization and its blockade suppresses the glutamate induced internalization of GLT-1, both in astrocytes and in a more straightforward experimental system like HEK293 cells transiently transfected with GLT-1. This regulatory mechanism might be relevant to control the amount of GLT-1 transporter at the cell surface in conditions like ischemia or traumatic brain injury, where extracellular concentrations of glutamate are persistently elevated and they promote rapid Ca2+ mobilization.
Mahsa Jarahzadeh - One of the best experts on this subject based on the ideXlab platform.
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Original Article Effects of A Voltage Sensitive Calcium Channel Blocker and A Sodium-Calcium Exchanger Inhibitor on Apoptosis of Motor Neurons in Adult Spinal Cord Slices
2016Co-Authors: Hamid Reza Momeni, Ph. D, Mahsa JarahzadehAbstract:Objective: The apoptosis of motor neurons is a critical phenomenon in spinal cord inju-ries. Adult spinal cord slices were used to investigate whether voltage sensitive calcium channels and Na+/Ca2+ Exchangers play a role in the apoptosis of motor neurons. Materials and Methods: In this experimental research, the thoracic region of the adult mouse spinal cord was sliced using a tissue chopper and the slices were incubated in a culture medium in the presence or absence of N/L type voltage sensitive calcium chan-nels blocker (loperamide, 100 µM) or Na+/Ca2+ Exchangers inhibitor(bepridil, 20 µM) for 6 hours. 3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyl tetrazolium (MTT) staining was used to assess slice viability while morphological features of apoptosis in motor neurons were studied using fluorescent staining. Results: After 6 hours in culture, loperamideand bepridil not only increased slice viability, but also prevented motor neuron apoptosis and significantly increased the percentage of viable motor neurons in the ventral horns of the spinal cord. Conclusion: The results of this study suggest that voltage sensitive calcium channels and Na+/Ca2+ Exchanger might be involved in the apoptosis of motor neurons in adult spinal cord slices
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effects of a voltage sensitive calcium channel blocker and a sodium calcium Exchanger inhibitor on apoptosis of motor neurons in adult spinal cord slices
Cell, 2012Co-Authors: Hamid Reza Momeni, Mahsa JarahzadehAbstract:Objective: The apoptosis of motor neurons is a critical phenomenon in spinal cord injuries. Adult spinal cord slices were used to investigate whether voltage sensitive calcium channels and Na+/Ca2+ Exchangers play a role in the apoptosis of motor neurons.
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Effects of A Voltage Sensitive Calcium Channel Blocker and A Sodium-Calcium Exchanger Inhibitor on Apoptosis of Motor Neurons in Adult Spinal Cord Slices
Royan Institute (ACECR) Tehran, 2012Co-Authors: Hamid Reza Momeni, Mahsa JarahzadehAbstract:Objective: The apoptosis of motor neurons is a critical phenomenon in spinal cord injuries. Adult spinal cord slices were used to investigate whether voltage sensitive calcium channels and Na+/Ca2+ Exchangers play a role in the apoptosis of motor neurons.Materials and Methods: In this experimental research, the thoracic region of the adult mouse spinal cord was sliced using a tissue chopper and the slices were incubated in a culture medium in the presence or absence of N/L type voltage sensitive calcium channels blocker (loperamide, 100 μM) or Na+/Ca2+ Exchangers inhibitor(bepridil, 20 μM) for 6 hours. 3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyl tetrazolium (MTT) staining was used to assess slice viability while morphological features of apoptosis in motor neurons were studied using fluorescent staining.Results: After 6 hours in culture, loperamideand bepridil not only increased slice viability, but also prevented motor neuron apoptosis and significantly increased the percentage of viable motor neurons in the ventral horns of the spinal cord.Conclusion: The results of this study suggest that voltage sensitive calcium channels and Na+/Ca2+ Exchanger might be involved in the apoptosis of motor neurons in adult spinal cord slices
Cecilio Gimenez - One of the best experts on this subject based on the ideXlab platform.
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activity dependent internalization of the glutamate transporter glt 1 requires calcium entry through the ncx sodium calcium Exchanger
Neurochemistry International, 2019Co-Authors: Ignacio Ibanez, David Bartolomemartin, Dolores Piniella, Cecilio Gimenez, Francisco ZafraAbstract:Abstract GLT-1 is the main glutamate transporter in the brain and its trafficking controls its availability at the cell surface, thereby shaping glutamatergic neurotransmission under physiological and pathological conditions. Extracellular glutamate is known to trigger ubiquitin-dependent GLT-1 internalization from the surface of the cell to the intracellular compartment, yet here we show that internalization also requires the participation of calcium ions. Consistent with previous studies, the addition of glutamate (1 mM) to mixed primary cultures (containing neurons and astrocytes) promotes GLT-1 internalization, an effect that was suppressed in the absence of extracellular Ca2+. The pathways of Ca2+ mobilization by astrocytes were analyzed in these mixed cultures using the genetically encoded calcium sensor GCaMP6f. A complex pattern of calcium entry was activated by glutamate, with a dramatic and rapid rise in the intracellular Ca2+ concentration partially driven by glutamate transporters, especially in the initial stages after exposure to glutamate. The Na+/Ca2+ Exchanger (NCX) plays a dominant role in this Ca2+ mobilization and its blockade suppresses the glutamate induced internalization of GLT-1, both in astrocytes and in a more straightforward experimental system like HEK293 cells transiently transfected with GLT-1. This regulatory mechanism might be relevant to control the amount of GLT-1 transporter at the cell surface in conditions like ischemia or traumatic brain injury, where extracellular concentrations of glutamate are persistently elevated and they promote rapid Ca2+ mobilization.
