The epsilon isoform of protein kinase C is involved in regulation of the LTD(4)-induced calcium signal in human intestinal epithelial cells
| Autor: | Christer Larsson, Charles Kumar Thodeti, Sailaja Paruchuri, Christian Kamp Nielsen, Anita Sjölander |
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| Rok vydání: | 2001 |
| Předmět: |
Gene isoform
Leukotriene D4 Microinjections Blotting Western chemistry.chemical_element Alpha (ethology) Down-Regulation Protein Kinase C-epsilon Biology Calcium Cell Fractionation Antibodies Cell Line chemistry.chemical_compound Western blot medicine Humans Calcium Signaling Enzyme Inhibitors Intestinal Mucosa Microinjection Protein kinase C Protein Kinase C medicine.diagnostic_test Dose-Response Relationship Drug Reverse Transcriptase Polymerase Chain Reaction Cell Membrane Cell Biology Molecular biology Epithelium Isoenzymes Protein Kinase C-delta Protein Transport medicine.anatomical_structure chemistry Tetradecanoylphorbol Acetate |
| Zdroj: | Experimental cell research. 262(2) |
| ISSN: | 0014-4827 |
| Popis: | We investigated the potential roles of specific isoforms of protein kinase C (PKC) in the regulation of leukotriene D(4)-induced Ca(2+) signaling in the intestinal epithelial cell line Int 407. RT-PCR and Western blot analysis revealed that these cells express the PKC isoforms alpha, betaII, delta, epsilon, zeta, and mu, but not betaI, gamma, eta, or theta;. The inflammatory mediator leukotriene D(4) (LTD(4)) caused the TPA-sensitive PKC isoforms alpha, delta, and epsilon, but not betaII, to rapidly translocate to a membrane-enriched fraction. The PKC inhibitor GF109203X at 30 microM but not 2 microM significantly impaired the LTD(4)-induced Ca(2+) signal, indicating that the response involves a novel PKC isoform, such as delta or epsilon, but not alpha. LTD(4)-induced Ca(2+) signaling was significantly suppressed in cells pretreated with TPA for 15 min and was abolished when the pretreatment was prolonged to 2 h. Immunoblot analysis revealed that the reduction in the LTD(4)-induced calcium signal coincided with a reduction in the cellular content of PKCepsilon and, to a limited extent, PKCdelta. LTD(4)-induced Ca(2+) signaling was also markedly suppressed by microinjection of antibodies against PKCepsilon but not PKCdelta. These data suggest that PKCepsilon plays a unique role in regulation of the LTD(4)-dependent Ca(2+) signal in intestinal epithelial cells. |
| Databáze: | OpenAIRE |
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