The immunomodulatory protein SV-IV protects serum-deprived cells against apoptosis but not against G0/G1 arrest: possible implications for the survival of implanting embryo

J Cell Physiol. 2007 Sep;212(3):610-25. doi: 10.1002/jcp.21058.

Abstract

Serum deprivation induced in human lymphoblastoid Raji cells oxidative stress-associated apoptotic death and G0/G1 cell cycle arrest. Addition into culture medium of the immunomodulatory protein Seminal vesicle protein 4 (SV-IV) protected these cells against apoptosis but not against cycle arrest. The antiapoptotic activity was related to: (1) decrease of endocellular reactive Oxygen species (ROS) (2) increase of mRNAs encoding anti-oxidant enzymes (catalase, G6PD) and antiapoptotic proteins (survivin, cox-1, Hsp70, c-Fos); (3) decrease of mRNAs encoding proapoptotic proteins (c-myc, Bax, caspase-3, Apaf-1). The biochemical changes underlaying these effects were probably induced by a protein tyrosine kinase (PTK) activity triggered by the binding of SV-IV to its putative plasma membrane receptors. The ineffectiveness of SV-IV to abrogate the cycle arrest was accounted for by its downregulating effects on D1,3/E G1-cyclins and CdK2/4 gene expression, ppRb/pRb ratio, and intracellular ROS concentration. In conclusion, these experiments: (1) prove that SV-IV acts as a cell survival factor; (2) suggest the involvement of a PTK in SV-IV signaling; (3) point to cell cycle-linked enzyme inhibition as responsible for cycle arrest; (4) provide a model to dissect the cycle arrest and apoptosis induced by serum withdrawal; (5) imply a possible role of SV-IV in the survival of hemiallogenic implanting embryos.

MeSH terms

  • Animals
  • Antioxidants / metabolism*
  • Antioxidants / pharmacology
  • Apoptosis Regulatory Proteins / genetics
  • Apoptosis Regulatory Proteins / metabolism
  • Apoptosis* / drug effects
  • Catalase / genetics
  • Catalase / metabolism
  • Cell Line, Tumor
  • Cell Proliferation* / drug effects
  • Culture Media, Serum-Free / metabolism
  • Cyclin-Dependent Kinases / metabolism
  • Cyclins / metabolism
  • Cytotoxicity, Immunologic
  • DNA Fragmentation
  • Embryo Culture Techniques
  • Embryo Implantation* / drug effects
  • Embryonic Development
  • G1 Phase* / drug effects
  • Genomic Instability
  • Glucosephosphate Dehydrogenase / genetics
  • Glucosephosphate Dehydrogenase / metabolism
  • Humans
  • Killer Cells, Natural / immunology
  • Killer Cells, Natural / metabolism
  • Leukocytes, Mononuclear / drug effects
  • Leukocytes, Mononuclear / enzymology
  • Leukocytes, Mononuclear / immunology
  • Leukocytes, Mononuclear / metabolism*
  • Mice
  • Mice, Inbred BALB C
  • Oxidative Stress
  • Phosphorylation
  • Protein-Tyrosine Kinases / metabolism
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Wistar
  • Reactive Oxygen Species / metabolism
  • Resting Phase, Cell Cycle* / drug effects
  • Retinoblastoma Protein / metabolism
  • Seminal Vesicle Secretory Proteins / metabolism*
  • Seminal Vesicle Secretory Proteins / pharmacology
  • Serum / metabolism
  • Signal Transduction
  • Time Factors

Substances

  • Antioxidants
  • Apoptosis Regulatory Proteins
  • Culture Media, Serum-Free
  • Cyclins
  • RNA, Messenger
  • Reactive Oxygen Species
  • Retinoblastoma Protein
  • Seminal Vesicle Secretory Proteins
  • Svs4 protein, rat
  • Glucosephosphate Dehydrogenase
  • Catalase
  • Protein-Tyrosine Kinases
  • Cyclin-Dependent Kinases