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High zinc status in lung cells slows growth and induces DNA damage-induced gene expression
Date:2/25/2008

doctoral graduate, designed the study to determine the influence of zinc status on Gadd45 expression and cell cycle progression in NHBE cells, and to decipher the molecular mechanism(s) exerted by the suppression of Gadd45 expression on cell growth and cell cycle progression in this normal human cell type.

Inhibition of cell growth, up-regulation of Gadd45 mRNA and protein expression, and blockage of G2/M cell cycle progression were observed in NHBE cells cultured in high zinc medium - the zinc supplemented (ZS) cells said Lei. The siRNA-mediated knocking down of Gadd45 was found to relieve G2/M blockage in ZS cells, which indicated that the blockage was Gadd45 dependent. Moreover, the enhanced phosphorylation of p38 and p53 (ser15) observed in ZS cells was normalized after suppression of Gadd45 by siRNA, implicating that the enhanced phosphorylation of these proteins was Gadd45 dependent. Thus, the researchers demonstrated for the first time that an elevated zinc status modulated the p53 and p38 signal transduction pathways to produce a delay at G2/M during cell cycle progression in NHBE cells.

Lei says the use of normal human cell types to evaluate the influence of nutrients and bioactive plant materials on the expression of stress responsive genes and cell cycle progression is a rapid and valuable approach to identify potential targets and provide mechanistic data. However, the applicability of these in vitro mechanistic data would require confirmation by detailed in vivo studies

Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine said This study on the molecular and cellular response of NHBE cells to a high zinc challenge may have important implications for conditions such as industrial exposure and extensive usage of zinc supplementation in animal production and in humans. He further stated The use of molecular and cellular approaches to address problems in nutritional sciences is the type of interdisc
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Contact: David K.Y. Lei
dlei@mail.umd.edu
301-405-2143
Society for Experimental Biology and Medicine
Source:Eurekalert

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