Collapsin response mediator protein-2 is highly expressed in the adult brain and it has been speculated to play roles in nervous system diseases. Studies determined for the first time whether collapsin response mediator protein-2 expression is altered in brain ischemia. We observed ischemia-modulated expression of different-sized collapsin response mediator protein-2. As the ischemic duration increased, the expression level of a known major 62 kDa collapsin response mediator protein-2 was decreased, whereas the expression of a newly-detected 58 kDa collapsin response mediator protein-2 was clearly increased in middle carotid artery-occluded rat brain tissues. Analysis of the two collapsin response mediator protein-2 bands revealed that the novel 58 kDa collapsin response mediator protein-2 observed in middle carotid artery-occluded rat brain tissues was a cleavage form; the predicted cleavage site is located at the carboxy-terminal of the collapsin response mediator protein-2. These data suggest that collapsin response mediator protein-2 is an important candidate controlling ischemic stroke.
Epigallocatechin gallate (EGCG), a well-known antioxidant molecule, has been reported to cause hepatotoxicity when used in excess. However, the mechanism underlying EGCG-induced hepatotoxicity is still unclear. To better understand the mode of action of EGCG-induced hepatotoxicity, we examined the effect of EGCG on human hepatic gene expression in HepG2 cells using microarrays. Analyses of microarray data revealed more than 1300 differentially expressed genes with a variety of biological processes. Upregulated genes showed a primary involvement with protein-related biological processes, such as protein synthesis, protein modification, and protein trafficking, while downregulated genes demonstrated a strong association with lipid transport. Genes involved in cellular stress responses were highly upregulated by EGCG treatment, in particular genes involved in endoplasmic reticulum (ER) stress, such as GADD153, GADD34, and ATF3. In addition, changes in genes responsible for cholesterol synthesis and lipid transport were also observed, which explains the high accumulation of EGCG-induced lipids. We also identified other regulatory genes that might aid in clarifying the molecular mechanism underlying EGCG-induced hepatotoxicity.
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