David K Lei

RESEARCH FOCUS

• Nutrient control of gene expression
• Elucidation of the mechanisms responsible for the altered gene expression modulated by cellular zinc status.
• Studies are being conducted to examine the influence of zinc status on the expression of tumor suppressor p53 gene and its target genes (p21, Gadd45 and Mdm2), as well as on cell cycle regulation and apoptosis, in normal human bronchial epithelial, prostate epithelial and aortic endothelial cells, and in human tumor cell lines.
• Influence of food and medicinal plant materials with bioactivities on cell cycle modulation and on tumor suppressor genes in normal human prostate epithelial cells and prostate tumor cell lines

Curriculum Vitae:

• Education:
  • Ph.D. in Nutrition, Michigan State University. 1973. East Lansing, Michigan.
  • M.S. in Nutrition, University of Guelph, Guelph, Ontario, Canada. 1970.
  • B.S in Nutrition, University of London, London, United Kingdom. 1968.
  Principal Academic Responsibilities:
  • NFSC 440: Advanced Human Nutrition
  • NFSC 660: Research Methods
  Research Activities: Dr. Lei as PI has acquired a total of more than $11 million in funding, during his career, with ~$2.3 million in federal competitive grant awards. Current research is focused in the area of nutrient control of gene expression. Major efforts are being devoted to the elucidation of the mechanisms responsible for the altered gene expression modulated by cellular zinc status. Studies are being conducted to examine the influence of zinc status on the expression of tumor suppressor p53 gene and its target genes (p21, Gadd45 and Mdm2), as well as on cell cycle regulation and apoptosis, in normal human bronchial epithelial, prostate epithelial and aortic endothelial cells, and in human tumor cell lines. A new program was initiated in 2006 to examine the influence of food and medicinal plant materials with bioactivities on cell cycle modulation and on tumor suppressor genes in normal human prostate epithelial cells and prostate tumor cell lines. In mid 2008, Lei as director of equipment acquisition initiated the establishment of a new nutritional sciences biotechnology lab (NSB lab) at King Saud University (KSU), Riyadh, Saudi Arabia. In late 2009, Lei as PI of a collaborative research program, on target delivery of bioactives by nano particles, between the NSB lab and the Chinese Academy of Sciences’ Nano Science Center in Beijing, was recommended for funding by KSU. Representative Publications: (Books)
  • Lei K.Y. 1991. "Dietary copper: Cholesterol and lipoprotein metabolism," in Annual Review of Nutrition, edited by R.E. Olson, D.M. Bier, and D.B. McCormick, Annual Reviews, Inc., Palo Alto, CA, Vol. 11, pp. 265 283.
  • Lei, K.Y. (Editor/Author). 1990. Role of Copper in Lipid Metabolism. CRC Press, Boca Raton, Florida (287 pages).
  (Journals)
  • Shih RS, Wong SHK, Schoene NW, and Lei KY (2010). Enhanced Gadd45 expressions and impaired G2/M progression are p53 dependent in zinc supplemented human bronchial epithelial cells. Exp Biol Med. 235: 932-940.
  • Alshatwi AA, Al Obaaid MA, Al Sedairy SA, Al-Assaf AH, Zhang JJ, and Lei KY (2010). Tomato powder is more protective than lycopene supplement against lipid peeroxidation in rats. Nutr. Res. 30: 66 – 73.
  • Han CT, Schoene NW, and Lei KY (2009). The influence of zinc deficiency on Akt-Mdm2-p53 and Akt-p21 signaling axes in normal and malignant human prostate cells, respectively. Am. J. Physiol. Cell Physiol. 297: 1188-1199.
  • Zhang JJ, Wu M, Schoene NW, Cheng WH, Wang TTY, Alshatwi AA, Alsaif M and Lei KY (2009). The effect of resveratrol and zinc on intracellular zinc status in normal human prostate (NHPrE) cells. Am J Physiol Cell Physiol. 297:C632-C644.
  • Alsaif MA, Alhamdan AA, Alothman AM, Al-Attas, Hakim IA, Harris RB, and Lei KY (2008). Variations between diagnosed and undiagnosed Saudi Diabetics. New Egyptian J Med. 38: 131 – 142.
  • Wong SHK, Shih RSM, Schoene NW, Lei KY (2008). Zinc induced G2/M blockage is p53 and p21 dependent in normal human bronchial epithelial cells. Am J Physiol Cell Physiol. 293: C1342- C1349.
  • Shih RS, Wong SHK, Schoene NW, Lei KY(2008). Suppression of Gadd45 alleviates the G2/M blockage and the enhanced phosphorylation of p53 and p38 in zinc supplemented normal human bronchial epithelial cells. Exp Biol Med. 233: 317-327 (Feature article for March issue 2008).
  • Yoe C, Parish M, Eddy D, Lei KY, Paleg B, and Schwarz JG (2008). Risk Management. The value of the food defense plan. Food Safety. April issue, pp16-21, 62-62.
  • Wong SHK, Zhao YQ, Schoene NW, Han CT, Shih RSM, and Lei KY. 2007. Zinc deficiency depresses p21 gene expression: Inhibition of cell cycle progression is independent of the decrease in p21 protein level in HepG2 cells. Am. J. Physiol. Cell Physiol. 292: C2175- C2184.
  • Alshatwi A, Han CT, Schoene NW, and Lei KY. 2006. Nuclear accumulations of p53 and Mdm2 are accompanied by reductions in c-Abl and p300 in zinc depleted human hepatoblastoma cells. Exp. Biol. Med. 231: 611-618.
  • Fanzo JC, Reaves SK, Cui L, Zhu L, Wu JYJ,Lei KY. 2002. p53 protein and p21 mRNA levels and caspase-3 activity are altered by zinc status in aortic endothelial cells. Am. J. Physiol. Cell Physiol. 283:C631-C638.
  • Cui LB, Schoene NW, Zhu L, Fanzo JC, Alshatwi A, Lei KY. 2002. Zinc depletion reduced Egr-1 and HNF-3 expression and apolipoprotein A-I promoter activity in Hep G2 cells. Am. J. Physiol. Cell Physiol. 283: C623-C630.
  • Fanzo JC, Reaves SK, Cui L, Zhu L, Wu JYJ, Wang YR, Lei KY. 2001. Zinc status affects p53, gadd45, and c-fos, expression and caspase-3 activity in human bronchial epithelial cells. Am. J. Physiol. Cell Physiol. 281:C751-757.
  • Reaves SK, Wu JYJ, Wu Y, Fanzo JC, Wang YR, Lei PP, Lei KY. 2000. Regulation of intestinal apolipoprotein B mRNA editing level by a zinc deficient diet and cDNA cloning of editing protein in hamsters. J. Nutr. 130: 2166-2173.
  • Reaves SK, Fanzo JC, Arima K, Wu JYJ, Wang YR, Lei PP, Lei KY. 2000. Expression of the p53 tumor suppressor gene expression is upregulated by depletion of intracellular zinc in Hep G2 cells. J. Nutr. 130: 1688-1694.
  • Wu JYJ, Wu Y, Reaves SK, Wang YR, Lei PP, Lei KY. 1999. Apolipoprotein A-I gene expression is regulated by cellular zinc status in Hep G2 cells. Am. J. Physiol. 277 (Cell Physiol.46): C537-544.
  • Wu JYJ, Zhang JJ, Wang Y, Reaves SK, Wang YR, Lei PP, Lei KY. 1997. Regulation of apolipoprotein A-I gene expression in Hep G2 cells depleted of copper by cupruretic tetramine. Am. J. Physiol. 273 (Cell Physiol. 42): C1362-C1370.
  • Wang YR, Wu JYJ, Reaves SK, Lei KY 1996. Enhanced expression of hepatic genes in copper-deficient rats detected by messenger RNA differential display. J. Nutr. 126:1772-1781.
  Current Support:
  • USDA, CSREES; Lei, PI; Risk Analysis-based Food Defense Certification Program for Professional and Academic Audiences. $540,000 for 9/2006 to 9/2010.
  • King Saud University (KSU); Lei, PI Establishment of Biotech lab at KSU. ~ $1 million for 3/2008 to present.
  • DL Global Consulting LLC; Lei, Research Advisor; Postdoc Fellowship. $50,000 for 1/2009 to 2/2010.
  Professional Membership:
  • American Society for Nutrition
  • American Society for Cell Biology
  • American Physiological Society
  • American Heart Association, Council on Arteriosclerosis
  • Society for Experimental Biology and Medicine
  • American Dietetic Association
  International Activities:
  • External Examiner, Food and Nutritional Sciences, Chinese University of Hong Kong, Hong Kong, PRC (2004 - present).
  • Member, Board of Consultants, Center of Excellence in Biotechnology Research, King Saud University, Riyadh, Saudi Arabia (3/2008 – present).
  Awards and Honors:
  • Outstanding Faculty Award, Asian American Faculty and Staff Association, University of Arizona. 1999.
  • Pew Faculty Scholar in Nutrition Fellowship. Pew National Nutrition Program. 1990-1991.
  • Outstanding Alumni Award, Dept. of Food Science and Human Nutrition, Michigan State University. 1989.

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