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  • 1
    Electronic Resource
    Electronic Resource
    Induction of early growth response-1 gene by interleukin-1β and tumor necrosis factor-α in normal human bone marrow stromal and osteoblastic cells: regulation by a protein kinase C inhibitor (1996)
    Springer
    Molecular and cellular biochemistry 156 (1996), S. 69-77 
    Details
    ISSN: 1573-4919
    Keywords: human bone marrow stromal cells ; osteoblasts ; Egr-1 ; immediate-early gene ; interleukin-1 β tumor necrosis factor-α
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The early growth response-1 (Egr-1) gene has been identified as a nuclear transcriptional factor and implicated in the regulation of growth and differentiation of osteoblastic cells. In the present study, we investigated whether Egr-1 mRNA is expressed and induced by interleukin-1 β (IL-β) and tumor necrosis factor-α (TNF-α) in normal human bond marrow stromal (HBMS) and osteoblastic (HOB) cells. Results demonstrate a very low basal expression of Egr-1 mRNA which is induced by IL-1 β and TNF-α in a time- and dose-dependent manner. Egr-1 mRNA induction was detectable within 15 min, reached maximal by 60 min and thereafter declined to basal levels by 120 min. Induction of Egr-1 mRNA by IL-1β and TNF-α was completely inhibited by H-7 suggesting the mediation of protein kinase C. The induction by IL-1 β and TNF-α of Egr-1 mRNA was independent of de novo protein synthesis since this induction was also observed in the presence of protein synthesis inhibitor cycloheximide. Fetal bovine serum and cycloheximide also independently induced the Egr-1 mRNA. Actinomycin D experiments demonstrated that Egr-1 mRNA is degraded very rapidly with a half-life of 30 min. Our results demonstrate the expression of Egr-1 gene and its induction by IL-1β, and TNF-α in normal human bone marrow stromal (osteoprogenitor) and osteoblastic cells in primary cultures. Data also reveal that the expression of Egr-1 gene is inhibited by protein kinase C inhibitor H-7 suggesting that the activation of protein kinase C or other protein kinases resulting in the phosphorylation of specific transcription factor(s) is the first immediate early step in the induction of immediate-early Egr-1 gene by IL-1 β and TNF-α. Results also suggest that Egr-1 is an important mediator of IL-1 β and TNF-α action in normal human osteoblastic cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00239321
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  • 2
    Electronic Resource
    Electronic Resource
    Activation of c-Jun NH2-terminal kinases by interleukin-1β in normal human osteoblastic and rat UMR-106 cells (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 87-93 
    Details
    ISSN: 0730-2312
    Keywords: MAP kinase pathways ; JNK ; human osteoblasts ; interleukin-1β ; UMR-106 cells ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We recently demonstrated the activation of extracellular signal- regulated protein kinase 1 and 2 (ERK1 and ERK2) by IGF-1, FGF-2, and PDGF-BB in normal human osteoblastic (HOB) cells as well as in rat and mouse osteoblastic cells. In this report, we have examined whether c-Jun NH2-Terminal Kinase (JNK) pathway is activated by growth factors and interleukin-1β (IL-1β) in normal HOB and rat UMR-106 cells using immune-complex kinase assay and anti-active JNK antibody, which recognizes activated forms of both JNK1 and JNK2. Results have demonstrated the presence of JNK1 and JNK2 proteins in normal HOB and UMR-106 cells. Both JNK1 and JNK2 were activated by IL-1β. IL-1β preferentially activated JNK pathway in a dose- and time-dependent manner and had little effect on ERK pathway. On the other hand, FGF-2 did not activate JNK but most strongly activated ERK pathway. The activation of JNK was maximal at 20 min whereas maximal activation of ERK1 and ERK2 was observed within 10 min. Results have clearly demonstrated that IL-1β preferentially activates JNK pathway whereas FGF-2 activates ERK pathway in normal human and rat UMR-106 osteoblastic cells. J. Cell. Biochem. 69:87-93, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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