Effects of arsenic on cell proliferation and its related gene expression in human epidermal keratinocyte

Jun Gu; Xin-ling Bi; Qing-sheng Mi; Jun-hui Wen

doi:10.1007/BF02934406

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Effects of arsenic on cell proliferation and its related gene expression in human epidermal keratinocyte

OriginalPaper | Updated：2021-08-27

- Effects of arsenic on cell proliferation and its related gene expression in human epidermal keratinocyte
- Effects of arsenic on cell proliferation and its related gene expression in human epidermal keratinocyte
- 中国结合医学杂志（英文版） 2002年8卷第4期页码：284-286
- Affiliations：
  
  1. Department of Dermatology, Changhai Hospital of Second Military Medical University,Shanghai
  2. John Robarts Institute, West Ontario University,Canada
  3. Department of Laboratory Diagnosis, Changhai Hospital of Second Military Medical University, Changhai
- Author bio：
- Funds：
- DOI：10.1007/BF02934406
  中图分类号：
- 纸质出版日期：2002，
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Gu, J., Bi, Xl., Mi, Qs. et al. Effects of arsenic on cell proliferation and its related gene expression in human epidermal keratinocyte., CJIM 8, 284–286 (2002). https://doi.org/10.1007/BF02934406

Jun Gu, Xin-ling Bi, Qing-sheng Mi, et al. Effects of arsenic on cell proliferation and its related gene expression in human epidermal keratinocyte[J]. Chinese Journal of Integrative Medicine, 2002,8(4):284-286.
Gu, J., Bi, Xl., Mi, Qs. et al. Effects of arsenic on cell proliferation and its related gene expression in human epidermal keratinocyte., CJIM 8, 284–286 (2002). https://doi.org/10.1007/BF02934406 DOI：

Jun Gu, Xin-ling Bi, Qing-sheng Mi, et al. Effects of arsenic on cell proliferation and its related gene expression in human epidermal keratinocyte[J]. Chinese Journal of Integrative Medicine, 2002,8(4):284-286. DOI： 10.1007/BF02934406.

摘要

To study the effects of low concentration of arsenic (As2O3) on DNA synthesis and related transcription factor gene E2F1 expression in keratinocyte. Human epidermal keratinocyte (cell line HaCaT) cultured in vitro was used. After treatment with various concentrations of arsenic

DNA synthesis and E2F1 expression in HaCaT cells were detected by using3H-TdR method and RT-PCR. Arsenic caused a modest increase of keratinocyte DNA synthesis when the concentration reached the range within 0.5–16 nmol/L

but the amount of incorporated3H-TdR decreased and returned to baseline level when the concentration of arsenic increased to over 16 nmol/L. RT-PCR analysis showed the level of E2F1 mRNA was elevated in HaCaT cells with the increase of DNA synthesis. Arsenic of a certain concentration could increase DNA synthesis and enhance E2F1 expression in HaCaT cell line

which might be one of the pathological mechanisms of skin disease related to arsenic.

Abstract

which might be one of the pathological mechanisms of skin disease related to arsenic.

关键词

Arsenickeratinocytecell proliferationtranscription factor 1 combined with adenovirus E2 promotor

Keywords

Arsenickeratinocytecell proliferationtranscription factor 1 combined with adenovirus E2 promotor

references

Goering PL, Aposhian HV, Mass MJ, et al. The enigma of arsenic carcinogenesis: role of metabolism. Toxicol Sci 1999; 49(1): 5–14.

Kapahi P, Takahashi T, Natoli G, et al. Inhibition of NFkappaB activation by arsenite through reaction with a critical cysteine in the activation loop of IkappaB kinase. J Biol Chem 2000; 275(46): 36062–36066.

Vega L, Styblo M, Patterson R, et al. Differential effects of trivalent and pentavalent arsenicals on cell proliferation and cytokine secretion in normal human epidermal keratinocytes. Toxicol Appl Pharmacol 2001;172(3): 225–232.

Pierce AM, Gimenez-Conti IB, Schneider-Broussard R, et al. Increased E2F1 activity induces skin tumors in mice heterozygous and nullizygous for p53. Proc Natl Acad Sci 1998;95(15): 8858–8863.

Paramio JM, Segrelles C, Casanova ML, et al. Opposite functions for E2F1 and E2F4 in human epidermal keratinocyte differentiation. J Biol Chem 2000; 275 (52): 41219–41226.

Kowalid TF, DeGregore J, Schwarz JK, et al. E2F1 overexpression in quiescent fibroblasts leads to induction of cellular DNA synthesis and apoptosis. J Virol 1995; 69 (4): 2491–2500.

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