Programmed cell death 5 factor enhances triptolide-induced fibroblast-like synoviocyte apoptosis of rheumatoid arthritis.

To study the effect of programmed cell death 5 (PDCD5) on apoptosis of rheumatoid arthritis fibroblast-like synoviocyte (RAFLS) induced by triptolide.
Cultured synovial cells in vitro from RA patients were transfected with Ad-PDCD5. In protein level, expression of PDCD5 protein in Ad-PDCD5 transfected RAFLS was detected by Western blot. RAFLS transfected with Ad-PDCD5 were cultured in presence or absence of triptolide and RAFLs apoptosis was determined by flow cytometry.
Transfection of RAFLS with increasing concentration of Ad-PDCD5 (50-300 MOI) resulted in dose-dependent increase of PDCD5 production. Apoptotic cells percentage of no transfection group, Ad-null group and Ad-PDCD5 group were, respectively, (22.41 +/- 3.87)%, (28.77 +/- 12.97)%, and (48.87 +/- 12.69)%. Alternatively, transfection without triptolide stimuli had no effect. The data showed that gene transfection of PDCD5 alone without triptolide was not sufficient to activate RAFLS apoptosis; PDCD5 acted as an enhancer rather than inductor of apoptosis.
Overexpression of PDCD5 could enhance apoptosis of RA FLS induced by triptolide; PDCD5 may be a potential therapeutic target to RA.
AuthorsJun Jiang, Ning Wang, Zhenpeng Guan, L V Houshan
JournalArtificial cells, blood substitutes, and immobilization biotechnology (Artif Cells Blood Substit Immobil Biotechnol) Vol. 38 Issue 1 Pg. 38-42 ( 2010) ISSN: 1532-4184 [Electronic] England
PMID20047520 (Publication Type: Journal Article)
Chemical References
  • Apoptosis Regulatory Proteins
  • Diterpenes
  • Epoxy Compounds
  • Neoplasm Proteins
  • PDCD5 protein, human
  • Phenanthrenes
  • triptolide
  • Adenoviridae (genetics)
  • Apoptosis (drug effects, genetics)
  • Apoptosis Regulatory Proteins (genetics, metabolism)
  • Arthritis, Rheumatoid (metabolism, pathology, physiopathology)
  • Cell Separation
  • Cells, Cultured
  • Cloning, Molecular
  • Diterpenes (pharmacology)
  • Epoxy Compounds (pharmacology)
  • Fibroblasts (drug effects, metabolism, pathology)
  • Flow Cytometry
  • Genetic Vectors
  • Humans
  • Neoplasm Proteins (genetics, metabolism)
  • Phenanthrenes (pharmacology)
  • Synovial Membrane (metabolism, pathology)
  • Transfection

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