Protein kinase C (PKC) involvement in ischemia-induced neuronal damage has been investigated in superfused rat cerebral cortex slices submitted to 15 min of oxygen-glucose deprivation (OGD) and in primary cultures of rat cortical neurons exposed to 100 microM glutamate (GLU) for 10 min. OGD signific
Expression and translocation of protein kinase C isoforms in rat microglial and astroglial cultures
β Scribed by Natalia Slepko; Mario Patrizio; Giulio Levi
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 127 KB
- Volume
- 57
- Category
- Article
- ISSN
- 0360-4012
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β¦ Synopsis
Cellular distribution and activation by phorbol myristate acetate (PMA) of classical (β£, β€I, β€II,β₯), novel (β¦, β, , ), and atypical (, ) protein kinase C (PKC) isoforms were studied in cultured rat neonatal microglial and astroglial cells by Western blot analysis. Among the classical isoforms, only β€II was expressed in microglia and astrocytes in the same abundance. The expression of β€I in microglia was less abundant, while PKCβ£ was not detectable in this cell type. PKCβ₯ was absent in both cell populations. A different pattern of expression was also found for novel and atypical isoenzymes: Both cell types expressed β¦, , , , and isoforms, but PKCβ was absent in microglia and the expression of PKC and PKC in these cells was low compared to astrocytes. The pattern of PKC distribution in cytosolic and particulate fractions as well as activation by short (10 min) and prolonged (4 hr) PMA treatment in both cell types were similar. On the whole, in comparison with astrocytes, PKC in microglial cells was less expressed, both in terms of number of isoforms and level of expression. The microglial profile of PKC isoforms differed from that of rat peritoneal macrophages, which did express PKCβ£. Preliminary evidence suggests that the ability of PMA to enhance cyclic AMP responses in astrocytes, but not in microglia, is related to the different pattern of expression of PKCβ£ and PKCβ in the two cell types.
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