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Acta Physiologica Congress

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Acta Physiologica 2009; Volume 195, Supplement 667
XXXV Congress of The Spanish Society for Physiological Sciences
2/17/2009-2/20/2009
Valencia, Spain


ROLE OF BCL-2 IN GSH-MEDIATED GENE EXPRESSION
Abstract number: P122

Dasi1,3 F, Markovic2,3 J, Mora2,3 NJ, Garcia3 JL, Gimeno3 A, Lloret2,3 A, Fernandez-Romero1,2,3 T, Pallardo2,3 FV

1Fundacin Investigacin Hospital Clnico Universitario Valencia.
2Department of Physiology. School of Medicine. University of Valencia.
3CIBERER (Centro de Investigacin Biomdica en Red de Enfermedades Raras)

Background: 

Recent studies demonstrated that glutathione (GSH) is important in cell proliferation, apoptosis, immune modulation, detoxification and scavenging of reactive oxygen species. Moreover, it has been suggested that GSH plays an important role in intracellular cell signaling, possibly through regulation of nuclear gene expression. Recently, it has also been reported a relationship between cellular redox state and Bcl-2 and its over-expression has been suggested as a mechanism to regulate intracellular GSH levels and distribution.

Aims: 

This study was undertaken to investigate the possible relationship between Bcl-2 levels and GSH levels and its correlation with cell growth and regulation of antioxidant enzymes and telomerase.

Methods: 

Mouse fibroblasts 3T3 were transfected with either a Bcl-2 expression vector or a shBcl-2 silencing vector and G-418 resistant clonal cell lines were generated. In these cells GSH levels were measured and correlated with cell growth and telomerase and antioxidant enzymes expression.

Results: 

Our results show that Bcl-2 over-expressing cells have higher proliferation rates, higher levels of cellular GSH and elevated expression of antioxidant enzymes and telomerase compared with the control cells transfected with the vector alone. Conversely, Bcl-2 down-regulation is associated with lower proliferation rates, GSH depletion and lower expression of antioxidant enzymes and telomerase.

Conclusion: 

Our results suggest that GSH acts through a Bcl-2 dependent mechanism as a transcriptional regulator by altering the cellular redox status.

To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 195, Supplement 667 :P122

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