Enhanced expression of the protooncogenes c-myc and c-fos in normal and malignant renal growth

Vamvakas, Spyridon; Bittner, Detlef; Köster, U.

doi:10.1016/0378-4274(93)90053-z

Cited by 35 publications

(13 citation statements)

References 30 publications

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“…to initiate DNA synthesis (5). Earlier studies have shown that DCVC (500 µM) induced expression of c-myc and c-fos in porcine kidney LLC-PK1 cells in a time-dependent manner (36). Thus, our findings are consistent with the notion that a low dose of DCVC upregulates pro-mitogenic signaling pathways and hence renal tubule repair.…”

Section: What Molecular Mechanisms Stimulate Renal Repair Following Asupporting

confidence: 92%

Molecular Mechanisms of Renal Tissue Repair in Survival from Acute Renal Tubule Necrosis: Role of ERK1/2 Pathway

et al. 2003

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Our earlier studies with S-(1,2-dichlorovinyl)-L -cysteine (DCVC) showed that prior administration of a low priming dose of 15 mg/kg, IP to mice, given 72 hours before administration of a normally lethal dose of DCVC (75 mg/kg, IP) led to renal tubule necrosis, however sustained renal tubule regeneration was observed and these mice recovered from renal failure and survived. The objective of the present study was to investigate the role of extracellular signal-regulated kinase (ERK) pathway in this autoprotection model. Following the priming dose of DCVC, IL-6 protein and mRNA increased markedly as early as 1 hour after dosing, peaking at 3 hours with a 1.5-fold increase in plasma. Immunocytochemistry on kidney sections using specific antibodies against TGF-α, HB-EGF, EGFr, IGF-1Rβ, Grb-2, and phospho-p44/42 MAP kinase (ERK1/2) revealed a significantly higher staining of these molecules 3 to 72 hours after dosing, indicating up regulation of the ERK pathway. Following a lethal dose of DCVC (75 mg/kg) the early increase in these signaling molecules was not sustained, being markedly reduced 24 and 36 hours after dosing, leading to inhibition of S-phase DNA synthesis, cell division and renal tubule repair. In contrast, prior treatment with a low dose of DCVC, followed by a high dose led to a sustained stimulation of the renal ERK pathway, renal tubule regeneration and recovery from acute renal failure. These results suggest that a sustained activation of the ERK1/2 pathway may be a key factor in enabling a continued renal tubule repair and hence protection from the progressive phase of DCVC-induced acute renal tubular necrosis in the mouse.

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Section: What Molecular Mechanisms Stimulate Renal Repair Following Asupporting

confidence: 92%

Molecular Mechanisms of Renal Tissue Repair in Survival from Acute Renal Tubule Necrosis: Role of ERK1/2 Pathway

et al. 2003

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“…Our data are in agreement with a previous report that DCVC induces a prolonged increase in c-fos and c-myc comparison to mitogen activation (Vamvakas et al, 1993). This prolonged induction could be due to either trancriptional activation or posttranscriptional stabilization of mRNA (Bernstein and Ross, 1989;Atwater et al, 1990;Ransone and Verma, 1990).…”

Section: Discussionsupporting

confidence: 93%

Signalling the molecular stress response to nephrotoxic and mutagenic cysteine conjugates: Differential roles for protein synthesis and calcium in the induction of c‐fos and c‐myc mRNA in LLC‐PK1 cells

Chen

Liu

et al. 1994

Journal Cellular Physiology

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Nephrotoxic and mutagenic cysteine conjugates (NCC) are activated by the enzyme cysteine conjugate, beta-lyase, to reactive acylating species which bind covalently to cellular macromolecules. We now show that an early event after treatment of LLC-PK1 cells with NCC is the induction of mRNA for both c-fos and c-myc. Treatment with S-(1,2-dichlorovinyl)-L-cysteine (DCVC) induced c-fos (53-fold) and c-myc mRNA (20-fold) and increased transcription about 3-fold for both genes. Covalent binding was required for induction of both mRNAs. Dithiothreitol partially prevented induction of both c-fos and c-myc RNA. Buffering the DCVC-induced increase in cytosolic free calcium had no effect on c-fos mRNA, but partially blocked c-myc mRNA induction. Cycloheximide blocked the induction of c-myc mRNA in the absence of an effect on c-fos induction. The data suggest that the increase in c-fos mRNA is a primary response to DCVC toxicity and occurs without a requirement for protein synthesis or an increase in intracellular free calcium. In contrast, c-myc induction requires protein synthesis, suggesting that the presence of another primary response factor may regulate induction either transcriptionally or posttranscriptionally. The data suggest that different signalling pathways regulate induction of c-fos and c-myc mRNA in response to stress caused by reactive acylating species.

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“…Heavy metal associated with atmospheric particles may accumulate in human being via inhalation and respiratory deposition, which may cause adverse effects on human health such as neuropathies symptoms, increased blood pressure and anaemia symptoms, kidney damage and increase the risk of lung and renal cancer (Vamvakas et al, 1993;Ewan and Pamphlett, 1996;Abernathy et al, 1999;Laden et al, 2000;Damek-Poprawa and Sawicka-Kapusta, 2003;Knaapen et al, 2004;Kampa and Castanas, 2008;Ning and Sioutas, 2010;Fang et al, 2013). As one of the specific heavy metal sources, the iron and steel production source can emit high concentrations of Fe and heavy metal Zn, Mn, Pb and Cd in atmospheric particles (Querol et al, 2007;Amodio et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Characterization and Source Identification of Heavy Metals in Ambient PM10 and PM2.5 in an Integrated Iron and Steel Industry Zone Compared with a Background Site

Dai

et al. 2015

Aerosol Air Qual. Res.

154

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The purpose of this study is to characterize heavy metals in ambient PM 10 (particles with aerodynamic diameter below 10 µm) and PM 2.5 (particles with aerodynamic diameter below 2.5 µm) particles in a typical integrated iron and steel industry zone (HG) and a background site (ZWY) during February 2011 to January 2012 in the Yangtze River Delta (YRD) region, China. Twelve elements were measured to study their levels, size distribution and sources. At the two sampling sites, Fe was found as the dominated metal in the total detected metals in both particle sizes, followed by Zn and Pb. They were regarded as the marker elements of iron and steel production emission along with Cr and Mn. The concentrations of all measured heavy metals in HG were 1-3.53 times higher than those measured in ZWY. When compared with previous studies, the concentrations of steel related elements (Fe, Zn, Mn) in this work were significantly high. The highest correlation coefficient was observed in HG for Fe and Zn. Additionally, Cd was found as the most enriched heavy metal by the enrichment factor analysis, followed by Zn, Pb, and Cu. The main sources contributing to heavy metals at HG site were identified by principle component analysis: steel dust (including coal combustion of coal-fired power plant, coke making and steel making emission), vehicle emission and road re-suspension dust and soil dust. Besides, steel dust was also found as the possible source of heavy metals at ZWY site. The result suggested the steel dust has influence on the whole study area.

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Enhanced expression of the protooncogenes c-myc and c-fos in normal and malignant renal growth

Cited by 35 publications

References 30 publications

Molecular Mechanisms of Renal Tissue Repair in Survival from Acute Renal Tubule Necrosis: Role of ERK1/2 Pathway

Molecular Mechanisms of Renal Tissue Repair in Survival from Acute Renal Tubule Necrosis: Role of ERK1/2 Pathway

Signalling the molecular stress response to nephrotoxic and mutagenic cysteine conjugates: Differential roles for protein synthesis and calcium in the induction of c‐fos and c‐myc mRNA in LLC‐PK1 cells

Characterization and Source Identification of Heavy Metals in Ambient PM10 and PM2.5 in an Integrated Iron and Steel Industry Zone Compared with a Background Site

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