ABSTRACT
Mitochondria-associated endoplasmic reticulum membranes (MAM) provide an excellent scaffold for crosstalk between ER and mitochondria, which play an important role in Ca2+ homeostasis, oxidative stress, inflammation, mitochondrial morphological and functional regulation, lipid metabolism, apop-tosis, autophagy and other processes. With the in-depth research, the function of MAM and the pathophysiological mechanisms of ischemic stroke overlap highly. On the other hand, a variety of drugs or compounds protect against ischemic stroke by affecting MAM-related proteins. In this review, we summarize the critical role of MAM in ischemic stroke and the potential of MAM as one drug target for treating ischemic stroke.
ABSTRACT
Objective@#To elucidate the effect of taurine on neurotoxicity induced by Mn by investigating activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase and content of Mn and active calmodulin in manganese exposed rats.@*Methods@#156 male SD rats were randomly divided into 1 control group, 3 manganese exposed groups (10, 15, and 20 mg/kg respectively) , and 9 taurine intervened groups based on orthogonal design (doses of taurine intervention were 100, 150, and 200 mg/kg respectively) , with 12 rats in each group. After 12 weeks of exposure, all rats were decapitated and corpus striatums were removed, activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase and content of Mn and active calmodulin were analyzed.@*Results@#The corpus striatum Mn content of the 3 dose groups exposed to Mn and 9 taurine intervened groups were significantly higher than that of the control group (P<0.05) . Active calmodulin content in 10 mg/kg manganese exposed group was significantly higher than that of the control group (P<0.05) . 150 and 200 mg/kg of taurine could decrease active calmodulin content of the group exposed to 10 mg/kg of Mn (P<0.05) . The corpus striatum activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase of the 3 dose groups exposed to Mn were significantly lower than that of the control group (P<0.05) . 150 mg/kg of taurine could increase activities of Na+-K+-ATPase of the group exposed to 10 mg/kg of Mn (P<0.05) . 150 and 200 mg/kg of taurine could respectively improve activities of Ca2+-Mg2+-ATPase of the group exposed to 15, 10 mg/kg of Mn (P<0.05) .@*Conclusion@#Mn can decrease the rats corpus striatum activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase, effect level of active calmodulin in relation to dose of Mn, to a certain extent, taurine could regulate activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase and improve the level of active calmodulin.
ABSTRACT
The changes of cell ultra structure as well as Ca2+ homeostasis involved in the drought-induced maize leaf senescence was investigated. Meanwhile, many indicatives of leaf senescence including thiobarbituric acid reactive substance (MDA), electrolyte leakage (EL), and chlorophyll along with soluble proteins were also detected during the process. The Polyethylene glycol6000(PEG6000)-incubated detached leaves showed a slight increase in the MDA content and electrolyte leakage during the first 30 min of our detection, which was corresponded to an unobvious alteration of the cell ultrastructure. Other typical senescence parameters measured in whole leaf exhibited a moderate elevation as well. Thereafter, however, the EL and MDA rose to a large extent, which was correlated with a dramatic damage to the cell ultrastructure with concomitant sharp decrease in the chlorophyll and soluble proteins content. The deposits of calcium antimonite, being an indicator for Ca2+ localization, were observed in the vacuoles as well as intercellular spaces in the leaves grown under normal condition. Nevertheless, after PEG treatment, it was revealed a distinct increment of Ca2+ in the cytoplasm as well as chloroplasts and nuclei. Moreover, with long-lasting treatment of PEG to the detached leaves, the concentration of Ca2+ as described above showed a continuous increment which was consist with the remarked alteration of physiological parameters and severe damage to the ultrastructure of cells, all of which indicated the leaf senescence. Such drought-induced leaf senescence might result from a loss of the cell's capability to extrude Ca2+. All above findings give us a good insight into the important role of Ca2+ homeostasis in the process of leaf senescence accelerated by the drought stress.
Subject(s)
Calcium , Cellular Senescence , Droughts , Plant Leaves , Zea mays , Chlorophyll/analysis , Electrolytes , Homeostasis , Lipid Peroxidation , Mesophyll Cells , Stress, Physiological , Signal TransductionABSTRACT
PURPOSE: Ca2+ homeostasis plays an important role in myocardial cell injury induced by hypoxia-reoxygenation, and prevention of intracellular Ca2+ overload is key to cardioprotection. Even though thiopental is a frequently used anesthetic agent, little is known about its cardioprotective effects, particulary in association with Ca2+ homeostasis. We investigated whether thiopental protects cardiomyocytes against hypoxia-reoxygenation injury by regulating Ca2+ homeostasis. MATERIALS AND METHODS: Neonatal rat cardiomyocytes were isolated. Cardiomyocytes were exposed to different concentrations of thiopental and immediately replaced in the hypoxic chamber to maintain hypoxia. After 1 hour of exposure, a culture dish was transferred to the CO2 incubator and cells were incubated at 37degrees C for 5 hours. At the end of the experiments, the authors assessed cell protection using immunoblot analysis and caspase activity. The mRNA of genes involved in Ca2+ homeostasis, mitochondrial membrane potential, and cellular Ca2+ levels were examined. RESULTS: In thiopental-treated cardiomyocytes, there was a decrease in expression of the proapoptotic protein Bax, caspase-3 activation, and intracellular Ca2+ content. In addition, both enhancement of anti-apoptotic protein Bcl-2 and activation of Erk concerned with survival were shown. Furthermore, thiopental attenuated alterations of genes involving Ca2+ regulation and significantly modulated abnormal changes of NCX and SERCA2a genes in hypoxia-reoxygenated neonatal cardiomyocytes. Thiopental suppressed disruption of mitochondrial membrane potential (Delta Psi m) induced by hypoxia-reoxygenation. CONCLUSION: Thiopental is likely to modulate expression of genes that regulate Ca2+ homeostasis, which reduces apoptotic cell death and results in cardioprotection.