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• W2018375135 abstract "Previously, we reported that TGF-β2 regulates the C3 gene expression in a dose- and time-dependent manner in monocytes. To extend these studies, we examined the role of PKC in the TGF-β2-mediated induction of C3 expression by the human monocyte cell line, U937. Treatment of U937 cells with the PKC inhibitors, H7 and calphostin C, suppressed TGF-β2-mediated induction of C3 protein levels, but not mRNA levels, in a dose-dependent manner. At the highest concentrations of H7 and calphostin C, C3 protein levels were inhibited 50% and 93%, respectively, compared to control levels. Treatment of U937 cells with HA1004, a weak PKC inhibitor used as a control for H7, did not inhibit induction of C3 protein levels. Down-modulating PKC with a prolonged exposure of U937 cells to PMA also suppressed TGF-β2-mediated C3 protein induction by as much as 82%. Incubating cell extracts isolated from TGF-β2-treated U937 cells with the PKC substrate, MIBP(4–14), resulted in increased substrate phosphorylation compared to cell extracts isolated from untreated cells. Addition of calphostin C suppressed the increased substrate phosphorylation by TGF-β2. Furthermore, biosynthetic labeling of U937 cells treated with TGF-β2 and calphostin C demonstrated an accumulation of C3 protein within cell lysates compared to controls. Collectively, these studies suggest a role for PKC in the secretion of C3 protein during TGF-β2-mediated regulation of C3 expression in U937 cells." @default.
• W2018375135 created "2016-06-24" @default.
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• W2018375135 date "1998-01-01" @default.
• W2018375135 modified "2023-09-27" @default.
• W2018375135 title "Transforming growth factor-β2 regulates C3 secretion in monocytes through a protein kinase C-dependent pathway" @default.
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• W2018375135 doi "https://doi.org/10.1016/s0161-5890(98)80012-6" @default.
• W2018375135 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9683259" @default.
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