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Gene expression in crossed cerebellar diaschisis in a transient middle cerebral artery occlusion rat model

ABSTRACT: Gene expression in crossed cerebellar diaschisis in a transient middle cerebral artery occlusion rat model

PROVIDER: PRJNA604005 | ENA |

REPOSITORIES: ENA

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Gene expression in crossed cerebellar diaschisis in a transient middle cerebral artery occlusion rat model

Project description:Crossed cerebellar diaschisis (CCD) is hypoperfusion and hypometabolism in the contralateral cerebellar hemisphere caused by supratentorial lesion. We evaluated chronological change of cerebellar blood flow (CbBF) and gene expressions in cerebellum using a rat model of focal ischemic stroke.

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Cerebellar Blood Flow and Gene Expression in Crossed Cerebellar Diaschisis after Transient Middle Cerebral Artery Occlusion in Rats.

Project description:Crossed cerebellar diaschisis (CCD) is a state of hypoperfusion and hypometabolism in the contralesional cerebellar hemisphere caused by a supratentorial lesion, but its pathophysiology is not fully understood. We evaluated chronological changes in cerebellar blood flow (CbBF) and gene expressions in the cerebellum using a rat model of transient middle cerebral artery occlusion (MCAO). CbBF was analyzed at two and seven days after MCAO using single photon emission computed tomography (SPECT). DNA microarray analysis and western blotting of the cerebellar cortex were performed and apoptotic cells in the cerebellar cortex were stained. CbBF in the contralesional hemisphere was significantly decreased and this lateral imbalance recovered over one week. Gene set enrichment analysis revealed that a gene set for "oxidative phosphorylation" was significantly upregulated while fourteen other gene sets including "apoptosis", "hypoxia" and "reactive oxygen species" showed a tendency toward upregulation in the contralesional cerebellum. MCAO upregulated the expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in the contralesional cerebellar cortex. The number of apoptotic cells increased in the molecular layer of the contralesional cerebellum. Focal cerebral ischemia in our rat MCAO model caused CCD along with enhanced expression of genes related to oxidative stress and apoptosis.

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