ArticleMolecular and cellular biochemistry1996
Induction of early growth response-1 gene by interleukin-1 beta and tumor necrosis factor-alpha in normal human bone marrow stromal an osteoblastic cells: regulation by a protein kinase C inhibitor.
Article in Molecular and cellular biochemistry, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 28 citations in OpenAlex.
- Thyrotropin exacerbates insulin resistance by triggering macrophage inflammation in subclinical hypothyroidism.Experimental & molecular medicine · 2025Article
- Mitigation of Osteoclast-Mediated Arthritic Bone Remodeling By Short Chain Fatty Acids.Arthritis & rheumatology (Hoboken, N.J.) · 2024Article
- The JNK-EGR1 signaling axis promotes TNF-α-induced endothelial differentiation of human mesenchymal stem cells via VEGFR2 expression.Cell death and differentiation · 2023Article
- WNT11 is a direct target of early growth response protein 1.BMB reports · 2020Article
- Chrysoeriol Prevents TNFα-Induced CYP19 Gene Expression via EGR-1 Downregulation in MCF7 Breast Cancer Cells.International journal of molecular sciences · 2020Article
- Leptin is a direct transcriptional target of EGR1 in human breast cancer cells.Molecular biology reports · 2019Article
- Egr-1 contributes to IL-1-mediated down-regulation of peroxisome proliferator-activated receptor γ expression in human osteoarthritic chondrocytes.Arthritis research & therapy · 2012Article
- SOD1 Transcriptional and Posttranscriptional Regulation and Its Potential Implications in ALS.Neurology research international · 2011Article
- Identification of NF-kappa B-regulated genes induced by TNFalpha utilizing expression profiling and RNA interference.Oncogene · 2003Article
- Regulation of periodontal ligament cell functions by interleukin-1beta.Infection and immunity · 1998Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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 beta, (IL-beta) and tumor necrosis factor-alpha (TNF-alpha) in normal human bone marrow stromal (HBMS) and osteoblastic (HOB) cells. Results demonstrate a very low basal expression of Egr-I mRNA which is induced by IL-1 beta, and TNF-alpha 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-1 beta and TNF-alpha was completely inhibited by H-7 suggesting the mediation of protein kinase C. The induction by IL-1 beta and TNF-alpha 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-1 beta, and TNF-alpha 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 beta, and TNF-alpha. Results also suggest that Egr-1 is an important mediator of IL-1 beta and TNF-alpha action in normal human osteoblastic cells.
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