| 1. |
- Matsumoto, Shohei, et al.
(författare)
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Protein Kinase C-γ and Calcium/Calmodulin-Dependent Protein Kinase II-α Are Persistently Translocated to Cell Membranes of the Rat Brain during and after Middle Cerebral Artery Occlusion
- 2004
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Ingår i: Journal of Cerebral Blood Flow and Metabolism. - 0271-678X .- 1559-7016. ; 24:1, s. 54-61
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Tidskriftsartikel (refereegranskat)abstract
- The levels of protein kinase C-γ (PKC-γ) and the calcium/calmodulin-dependent kinase II-α (CaMKII-α) were measured in crude synaptosomal (P2), particulate (P3), and cytosolic (S3) fractions of the neocortex of rats exposed to 1-hour and 2-hour middle cerebral artery occlusion (MCAO) and 2-hour MCAO followed by 2-hour reperfusion. During MCAO, PKC levels increased in P2 and P3 in the most severe ischemic areas concomitantly with a decrease in S3. In the penumbra, PKCγ decreased in S3 without any significant increases in P2 and P3. Total PKC-γ also decreased in the penumbra but not in the ischemic core, suggesting that the protein is degraded by an energy-dependent mechanism, possibly by the 26S proteasome. The CaMKII-α levels increased in P2 but not P3 during ischemia and reperfusion in all ischemic regions, particularly in the ischemic core. Concomitantly, the levels in S3 decreased by 20% to 40% in the penumbra and by approximately 80% in the ischemic core. There were no changes in the total levels of CaMKII-α during MCAO. The authors conclude that during and after ischemia, PKC and CaMKII-α are translocated to the cell membranes, particularly synaptic membranes, where they may modulate cellular function, such as neurotransmission, and also affect cell survival. Drugs preventing PKC and/or CaMKII-α translocation may prove beneficial against ischemic cell death.
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| 2. |
- Sakai, Takao, et al.
(författare)
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Plasma fibronectin supports neuronal survival and reduces brain injury following transient focal cerebral ischemia but is not essential for skin-wound healing and hemostasis
- 2001
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Ingår i: Nature Medicine. - : Springer Science and Business Media LLC. - 1546-170X .- 1078-8956. ; 7:3, s. 324-330
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Tidskriftsartikel (refereegranskat)abstract
- Fibronectin performs essential roles in embryonic development and is prominently expressed during tissue repair. Two forms of fibronectin have been Identified: plasma fibronectin (pFn), which Is expressed by hepatocytes and secreted In soluble form into plasma; and cellular fibronectin (cFn), an insoluble form expressed locally by fibroblasts and other cell types and deposited and assembled into the extracellular matrix. To investigate the role of pFn in vivo, we generated pfn-deficient adult mice using Cre-loxP conditional gene-knockout technology. Here we show that pfn-deficient mice show increased neuronal apoptosis and larger Infarction areas following transient focal cerebral ischemia. However, pFn is dispensable for skin-wound healing and hemostasis.
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