Overexpression of regucalcin suppresses cell death in cloned rat hepatoma H4-II-E cells induced by tumor necrosis factor-alpha or thapsigargin

J Cell Biochem. 2004 May 15;92(2):296-306. doi: 10.1002/jcb.20056.

Abstract

The role of regucalcin, which is a regulatory protein in intracellular signaling pathway, in the regulation of cell death was investigated by using the cloned rat hepatoma H4-II-E cells overexpressing regucalcin. The hepatoma cells (wild-type) and stable regucalcin (RC)/pCXN2 transfectants were cultured for 72 h in medium containing 10% fetal bovine serum (FBS) to obtain subconfluent monolayers. The proliferation of the cells was significantly suppressed in transfectants cultured for 72 h, as shown previously (Tsurusaki and Yamaguchi [2003]: J Cell Biochem 90:619-626). After culture for 72 h, cells were further cultured for 24-72 h in medium without FBS containing either vehicle, tumor necrosis factor-alpha (TNF-alpha; 0.1, 1, or 10 ng/ml) or thapsigargin (10(-7)-10(-5) M). The number of wild-type cells was significantly decreased by culture for 42 or 72 h in the presence of TNF-alpha (0.1, 1, or 10 ng/ml) or thapsigargin (10(-7)-10(-5) M). The effect of TNF-alpha (0.1 or 1 ng/ml) or thapsigargin (10(-7) or 10(-6) M) in decreasing the number of hepatoma cells was significantly prevented in transfectants overexpressing regucalcin. The presence of TNF-alpha (10 ng/ml) or thapsigargin (10(-5) M) caused a significant decrease in cell number of transfectants. Ca(2+)/calmodulin-dependent nitric oxide (NO) synthase activity in wild-type cells was significantly increased by culture with TNF-alpha (10 ng/ml) for 48 or 72 h. This increase was significantly prevented in transfectants. Culture with thapsigargin (10(-5) M) caused a significant increase in Ca(2+)/calmodulin-dependent NO synthase activity in wild-type cells or transfectants. TNF-alpha-induced decrease in the number of wild-type cells was significantly prevented by culture with N omega-nitro-L-arginine (10(-4) M), an inhibitor of caspase. Agarose gel electrophoresis showed the presence of low-molecular-weight deoxyribonucleic acid (DNA) fragments of adherent wild-type cells cultured with thapsigargin (10(-6) M), and this DNA fragmentation was not suppressed by culture with caspase inhibitor. Thapsigargin-induced DNA fragmentation was significantly suppressed in transfectants cultured with or without caspase inhibitor. This study demonstrates that overexpression of regucalcin has a suppressive effect on cell death induced by TNF-alpha or thapsigargin.

MeSH terms

  • Animals
  • Apoptosis* / drug effects
  • Calcium-Binding Proteins / genetics
  • Calcium-Binding Proteins / metabolism*
  • Carboxylic Ester Hydrolases
  • Caspase Inhibitors
  • Caspases / metabolism
  • Cell Line, Tumor
  • Enzyme Inhibitors / pharmacology
  • Gene Expression Regulation, Neoplastic*
  • Intracellular Signaling Peptides and Proteins
  • Liver Neoplasms / genetics
  • Liver Neoplasms / metabolism*
  • Liver Neoplasms / pathology*
  • Nitric Oxide Synthase / metabolism
  • Rats
  • Sulfotransferases
  • Thapsigargin / pharmacology*
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Calcium-Binding Proteins
  • Caspase Inhibitors
  • Enzyme Inhibitors
  • Intracellular Signaling Peptides and Proteins
  • Tumor Necrosis Factor-alpha
  • Thapsigargin
  • Nitric Oxide Synthase
  • Sulfotransferases
  • alcohol sulfotransferase
  • Carboxylic Ester Hydrolases
  • Rgn protein, rat
  • Caspases