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Retinoid x receptor agonists increase bcl2a1 expression and decrease apoptosis of naive T lymphocytes.

Reuven Rasooly1, Gertrud U Schuster, Jeffrey P Gregg

  • 1U.S. Department of Agriculture (USDA) Western Human Nutrition Research Center and Nutrition Department, University of California, Davis, CA, 95616, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|December 13, 2005
PubMed
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Retinoid X receptor (RXR) agonists increase the expression of the antiapoptotic gene Bcl2a1 in T lymphocytes. This upregulation of Bcl2a1 by RXR agonists reduces T lymphocyte apoptosis, promoting cell survival.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Vitamin A metabolites, including all-trans-retinoic acid and 9-cis-retinoic acid, modulate T lymphocyte development and function.
  • Retinoic acid receptors (RARs) and retinoid X receptors (RXRs) are key nuclear receptors mediating the effects of retinoids.
  • Naive T lymphocytes express RAR-alpha, RXR-alpha, and RXR-beta, indicating sensitivity to retinoid signaling.

Purpose of the Study:

  • To identify retinoid X receptor (RXR)-responsive genes in naive T lymphocytes.
  • To investigate the role of RXR activation in regulating T lymphocyte apoptosis.
  • To elucidate the specific molecular mechanisms by which RXR agonists affect T cell survival.

Main Methods:

  • DNA microarray analysis to identify differentially expressed genes in T lymphocytes treated with an RXR agonist (AGN194204).

Related Experiment Videos

  • Quantitative real-time PCR to validate gene expression changes, specifically for Bcl2a1.
  • Luciferase reporter assays to assess Bcl2a1 promoter activity and Annexin V staining to measure apoptosis.

    • Main Results:

    • RXR agonist treatment resulted in differential expression of 128 genes, with 15% related to cell growth and apoptosis.
    • Bcl2a1, an antiapoptotic gene, was significantly upregulated by RXR agonists (AGN194204 and 9-cis-retinoic acid) in naive T lymphocytes.
    • RXR agonists decreased T lymphocyte apoptosis and increased Bcl2a1 promoter activity, without affecting Bcl2 and Bcl-xL expression.

    Conclusions:

    • RXR agonists directly enhance Bcl2a1 promoter activity and increase Bcl2a1 expression in naive T lymphocytes.
    • The observed decrease in T lymphocyte apoptosis upon RXR agonist treatment is likely mediated by the upregulation of Bcl2a1.
    • These findings highlight a novel mechanism by which retinoids influence T cell survival through specific regulation of Bcl2a1.