SS-A/Ro52 promotes apoptosis by regulating Bcl-2 production

Siti Nur Aisyah Jauharoh, Jun Saegusa, Takeshi Sugimoto, Bambang Ardianto, Shimpei Kasagi, Daisuke Sugiyama, Chiyo Kurimoto, Osamu Tokuno, Yuji Nakamachi, Shunichi Kumagai, Seiji Kawano

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20 Citations (Scopus)

Abstract

SS-A/Ro52 (Ro52), an autoantigen in systemic autoimmune diseases such as systemic lupus erythematosus and Sjögren's syndrome, has E3 ligase activity to ubiquitinate proteins that protect against viral infection. To investigate Ro52's role during stress, we transiently knocked it down in HeLa cells by siRo52 transfection. We found that Ro52 low HeLa cells were significantly more resistant to apoptosis than wild-type HeLa cells when stimulated by H 2O 2- or diamide-induced oxidative stress, IFN-α, IFN-γ and anti-Fas antibody, etoposide, or γ-irradiation. Furthermore, Ro52-mediated apoptosis was not influenced by p53 protein level in HeLa cells. Depleting Ro52 in HeLa cells caused Bcl-2, but not other Bcl-2 family molecules, to be upregulated. Taken together, our data showed that Ro52 is a universal proapoptotic molecule, and that its proapoptotic effect does not depend on p53, but is exerted through negative regulation of the anti-apoptotic protein Bcl-2. These findings shed light on a new physiological role for Ro52 that is important to intracellular immunity.

Original languageEnglish
Pages (from-to)582-587
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume417
Issue number1
DOIs
Publication statusPublished - 2012 Jan 6

Keywords

  • Apoptosis
  • Bcl-2
  • P53
  • SS-A/Ro52
  • TRIM21

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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  • Cite this

    Jauharoh, S. N. A., Saegusa, J., Sugimoto, T., Ardianto, B., Kasagi, S., Sugiyama, D., Kurimoto, C., Tokuno, O., Nakamachi, Y., Kumagai, S., & Kawano, S. (2012). SS-A/Ro52 promotes apoptosis by regulating Bcl-2 production. Biochemical and Biophysical Research Communications, 417(1), 582-587. https://doi.org/10.1016/j.bbrc.2011.12.010