Words similar to vacuolation
Example sentences for: vacuolation
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Peroxisomes shorten chains of very long fatty acids, unsaturated fatty acids and branched fatty acids by β-oxidation [ 60 61 ] . They play critical roles in synthesis of ether phospholipids and cholesterol [ 62 63 ] . Peroxisomal abundance is associated with high membrane demand such as myelination in the central nervous system [ 64 65 ] and peroxisome diseases result in defective myelination [ 66 ] . Because the outer mitochondrial membrane normally tightly wraps around mitochondria, the extension of the outer membrane during vacuolation requires new membranes.
Because mutant SOD1 is prone to unfold [ 31 32 33 34 ] and form aggregates [ 11 14 35 36 ] , it has been proposed that abnormal SOD1 aggregation generates toxicity [ 10 ] . To determine whether SOD1 aggregates are involved in mitochondrial vacuolation, we examined whether vacuoles contain SOD1 aggregates by immunofluorescence and immuno EM.
The absence of matrix expansion and the involvement of peroxisomes but not lysosomes together indicate that mutant SOD1-induced mitochondrial vacuolation is neither MPT nor autophagy.
Mutant SOD1 causes dysfunction and structural damage of mitochondria in cultured neuronal cells [ 18 19 20 ] and at early disease stages in mutant SOD1 transgenic mice [ 21 22 ] . Human ALS also shows mitochondrial damage, dysfunction and loss [ 23 24 ] . The mechanism whereby mutant SOD1 causes mitochondrial damage has not been determined, but recent evidence shows that mutant SOD1 is imported into mitochondria [ 21 25 26 ] , and this mitochondrial localization may cause direct damage to mitochondria and induce cell death [ 27 ] . Consistent with this possibility, previous work suggested that mitochondrial vacuolation was developed from expansion of the intermembrane space [ 17 ] . However, the possibility that the vacuoles represent autophagic vacuolation has not been ruled out, because the source of the vacuolar membrane was not known.
Our previous study showed that functional decline of mitochondria appears in the SOD1 G93Amice as early as 60 to 100 days of age [ 22 ] . This precedes the peak of mitochondrial vacuolation and the onset of the disease by two to three months [ 15 ] . Mitochondrial dysfunction can lead to energy deficiency and ionic imbalance [ 68 ] , elevated ROS and oxidative damage [ 69 ] , and increased sensitivity of neurons to excitotoxicity [ 19 70 71 72 ] . These effects could precipitate MVISE, which trigger cell death programs by releasing pro-apoptotic proteins resided in the mitochondrial intermembrane space, such as cytochrome c, AIF, SMAC/DIABLO, endo G and Htra/Omi [ 73 ] . The absence of cytochrome c in the porous large vacuoles and the presence of cytochrome c in the small vacuoles (Fig.
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