title: Transient elevation of synaptosomal mitoenergetic proteins and Hsp70 early in a rat model of chronic cerebrovascular hypoperfusion.
abstract: Chronic cerebral hypoperfusion (CCH) might account for the cognitive deficits associated with vascular cognitive impairment, but the mechanisms of hypoperfusion insulting to the cognition remain obscure. In the present study, Wistar rats underwent permanent occlusion of bilateral common carotid arteries to induce CCH. 2D-DIGE combined with MALDI-TOF MS was applied to determine the proteins that were differentially expressed in synaptosomes of prefrontal cortex and hippocampus. ATPsynβ, NDUFS1, UQCRC1 and Hsp70 were elevated both in synaptosomes of cortex and hippocampus at week 2 after operation, but subsided to baseline at week 4 except ATPsynβ which was still upregulated in synaptosomes of hippocampus at week 4. IDH3A and PDC-E2 were increased, respectively, in synaptosomes of prefrontal cortex and hippocampus at week 2, and showed no difference when compared to control at week 4. Malate dehydrogenase showed no difference in synaptosomes of prefrontal cortex and hippocampus at week 2, but showed an elevation in synaptosomes of prefrontal cortex at week 4. Our results imply that metabolic reserve and anti-oxidative stress might transiently exist in the early stage of CCH, which probably help cognitive save.
authors.affiliation: Department of Neurology, The First Hospital, Jilin University, 71 Xinmin Street, Changchun 130021, China.
authors.forename: Hai Ning
authors.initials: HN
authors.lastname: Zhang
authors.forename: Jiang
authors.initials: J
authors.lastname: Wu
authors.forename: Tao
authors.initials: T
authors.lastname: Jin
authors.forename: Ming
authors.initials: M
authors.lastname: Chang
authors.forename: Li
authors.initials: L
authors.lastname: Sun
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001921:Brain / Q000473:pathology* / Q000648:ultrastructure; D002561:Cerebrovascular Disorders / Q000378:metabolism* / Q000473:pathology; D002908:Chronic Disease; D003072:Cognition Disorders / Q000209:etiology; D004195:Disease Models, Animal; D045222:Electron Transport Chain Complex Proteins / Q000378:metabolism*; D015180:Electrophoresis, Gel, Two-Dimensional; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism*; D008291:Malate Dehydrogenase / Q000378:metabolism; D008297:Male; D025261:Mitochondrial Proton-Translocating ATPases / Q000378:metabolism; D009245:NADH Dehydrogenase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D019032:Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization; D013574:Synaptosomes / Q000378:metabolism*; D014451:Ubiquinone / Q000378:metabolism
chemical_list: D045222:Electron Transport Chain Complex Proteins; D018840:HSP70 Heat-Shock Proteins; D014451:Ubiquinone; D008291:Malate Dehydrogenase; D009245:NADH Dehydrogenase; C497342:ATP synthase beta subunit, rat; D025261:Mitochondrial Proton-Translocating ATPases