Na^(+)/K^(+)-ATPase is a transmembrane protein that has important roles in the maintenance of electrochemical gradients across cell membranes by transporting three Na^(+)out of and two K^(+)into cells.Additionally,Na^...Na^(+)/K^(+)-ATPase is a transmembrane protein that has important roles in the maintenance of electrochemical gradients across cell membranes by transporting three Na^(+)out of and two K^(+)into cells.Additionally,Na^(+)/K^(+)-ATPase participates in Ca^(2+)-signaling transduction and neurotransmitter release by coordinating the ion concentration gradient across the cell membrane.Na^(+)/K^(+)-ATPase works synergistically with multiple ion channels in the cell membrane to form a dynamic network of ion homeostatic regulation and affects cellular communication by regulating chemical signals and the ion balance among different types of cells.Therefo re,it is not surprising that Na^(+)/K^(+)-ATPase dysfunction has emerged as a risk factor for a variety of neurological diseases.However,published studies have so far only elucidated the important roles of Na^(+)/K^(+)-ATPase dysfunction in disease development,and we are lacking detailed mechanisms to clarify how Na^(+)/K^(+)-ATPase affects cell function.Our recent studies revealed that membrane loss of Na^(+)/K^(+)-ATPase is a key mechanism in many neurological disorders,particularly stroke and Parkinson's disease.Stabilization of plasma membrane Na^(+)/K^(+)-ATPase with an antibody is a novel strategy to treat these diseases.For this reason,Na^(+)/K^(+)-ATPase acts not only as a simple ion pump but also as a sensor/regulator or cytoprotective protein,participating in signal transduction such as neuronal autophagy and apoptosis,and glial cell migration.Thus,the present review attempts to summarize the novel biological functions of Na^(+)/K^(+)-ATPase and Na^(+)/K^(+)-ATPase-related pathogenesis.The potential for novel strategies to treat Na^(+)/K^(+)-ATPase-related brain diseases will also be discussed.展开更多
Experiments were conducted to examine the effects of salinity fluctuation frequency on the osmolarity, Na^＋-K^＋-ATPase activity and HSP70 of Chinese shrimp Fenneropenaeus chinensis ruth initial wet body weight of 1....Experiments were conducted to examine the effects of salinity fluctuation frequency on the osmolarity, Na^＋-K^＋-ATPase activity and HSP70 of Chinese shrimp Fenneropenaeus chinensis ruth initial wet body weight of 1.460g±0.091 g. The salinity in the control group （DO） was 28 throughout the experiment, whereas treatments D2, D4, D6 and D8 were subjected to different salinity fluctuation frequencies of 2, 4, 6 and 8d, respectively. The salinity in treatments D2, D4, D6 and D8 was kept at 28 for 2, 4, 6 and 8d, respectively, decreased abruptly to salinity 24, lasted for another 2 d, and then was raised to its initial value 28. This was a complete salinity fluctuation cycle that afterwards repeated itself. After 32 days, the osmolarity in treatments D2, D4, D6 and D8 was significantly lower than that in treatment DO （P〈0.05）. There were significant differences in both muscle and eyestalks HSP70 expression among groups. The HSP70 expressions in muscle and eyestalks in group D4 were 61.4% and 57.0% higher, respectively, than that in the control group DO （P〈0.05）. There were, however, no significant differences in gill or hepatopancreas Na^＋-K^＋-ATPase activity between the treatments and the control.展开更多
Changes in the activity of Na^+, K^+-ATPase and in the water, sodium, and potassium levels in the ischemic brain were investigated in rabbits 2, 4, and 24h following occlusion of middle cerebral artery (MCAo) and in s...Changes in the activity of Na^+, K^+-ATPase and in the water, sodium, and potassium levels in the ischemic brain were investigated in rabbits 2, 4, and 24h following occlusion of middle cerebral artery (MCAo) and in shamoccluded control. An increase in Na^+, K^+-ATPase activity was observed in 2h and 4h groups, with a subsequent decrease in the enzyme activity. The elevation in Na^+, K^+-ATPase activity was accompanied by an increase in the sodium content and a slight decrease in the potassium content. These changes are presumed to occure because of stimilated active transport of sodium from blood to brain across the brain capillaries. We suggest that the elevated activity of Na^+, K^+-A TPase may participate in the pathogenesis of ischemic brain edema.展开更多
基金supported by the National Natural Science Foundation of China,No.82173800 (to JB)Shenzhen Science and Technology Program,No.KQTD20200820113040070 (to JB)。
文摘Na^(+)/K^(+)-ATPase is a transmembrane protein that has important roles in the maintenance of electrochemical gradients across cell membranes by transporting three Na^(+)out of and two K^(+)into cells.Additionally,Na^(+)/K^(+)-ATPase participates in Ca^(2+)-signaling transduction and neurotransmitter release by coordinating the ion concentration gradient across the cell membrane.Na^(+)/K^(+)-ATPase works synergistically with multiple ion channels in the cell membrane to form a dynamic network of ion homeostatic regulation and affects cellular communication by regulating chemical signals and the ion balance among different types of cells.Therefo re,it is not surprising that Na^(+)/K^(+)-ATPase dysfunction has emerged as a risk factor for a variety of neurological diseases.However,published studies have so far only elucidated the important roles of Na^(+)/K^(+)-ATPase dysfunction in disease development,and we are lacking detailed mechanisms to clarify how Na^(+)/K^(+)-ATPase affects cell function.Our recent studies revealed that membrane loss of Na^(+)/K^(+)-ATPase is a key mechanism in many neurological disorders,particularly stroke and Parkinson's disease.Stabilization of plasma membrane Na^(+)/K^(+)-ATPase with an antibody is a novel strategy to treat these diseases.For this reason,Na^(+)/K^(+)-ATPase acts not only as a simple ion pump but also as a sensor/regulator or cytoprotective protein,participating in signal transduction such as neuronal autophagy and apoptosis,and glial cell migration.Thus,the present review attempts to summarize the novel biological functions of Na^(+)/K^(+)-ATPase and Na^(+)/K^(+)-ATPase-related pathogenesis.The potential for novel strategies to treat Na^(+)/K^(+)-ATPase-related brain diseases will also be discussed.
基金supported by funds from the National Natural Science Foundation of China (No. 30571441)the Project of The Talented Youth Scientist of Shandong Province (No. 2006BS07002)the National Eleventh Five-Year Scientific and Technological Key Project (No.2006BAD09A07).
文摘Experiments were conducted to examine the effects of salinity fluctuation frequency on the osmolarity, Na^＋-K^＋-ATPase activity and HSP70 of Chinese shrimp Fenneropenaeus chinensis ruth initial wet body weight of 1.460g±0.091 g. The salinity in the control group （DO） was 28 throughout the experiment, whereas treatments D2, D4, D6 and D8 were subjected to different salinity fluctuation frequencies of 2, 4, 6 and 8d, respectively. The salinity in treatments D2, D4, D6 and D8 was kept at 28 for 2, 4, 6 and 8d, respectively, decreased abruptly to salinity 24, lasted for another 2 d, and then was raised to its initial value 28. This was a complete salinity fluctuation cycle that afterwards repeated itself. After 32 days, the osmolarity in treatments D2, D4, D6 and D8 was significantly lower than that in treatment DO （P〈0.05）. There were significant differences in both muscle and eyestalks HSP70 expression among groups. The HSP70 expressions in muscle and eyestalks in group D4 were 61.4% and 57.0% higher, respectively, than that in the control group DO （P〈0.05）. There were, however, no significant differences in gill or hepatopancreas Na^＋-K^＋-ATPase activity between the treatments and the control.
基金This work was supported by a grant from National Seventh-Five Year Plan's Cerebrovascular Diseases Research Project
文摘Changes in the activity of Na^+, K^+-ATPase and in the water, sodium, and potassium levels in the ischemic brain were investigated in rabbits 2, 4, and 24h following occlusion of middle cerebral artery (MCAo) and in shamoccluded control. An increase in Na^+, K^+-ATPase activity was observed in 2h and 4h groups, with a subsequent decrease in the enzyme activity. The elevation in Na^+, K^+-ATPase activity was accompanied by an increase in the sodium content and a slight decrease in the potassium content. These changes are presumed to occure because of stimilated active transport of sodium from blood to brain across the brain capillaries. We suggest that the elevated activity of Na^+, K^+-A TPase may participate in the pathogenesis of ischemic brain edema.
