Published online 3 February 2004
Nucleic Acids Research, 2004, Vol. 32, No. 2 757-766
© 2004 Oxford University Press
Transcription regulation of TNF-
-early response genes by poly(ADP-ribose) polymerase-1 in murine heart endothelial cells
1 Transplant Unit, University Hospital ‘Virgen de la Arrixaca’, Murcia, Spain, 2 Department of Immunology, University Hospital ‘Virgen de la Arrixaca’, Murcia, Spain, 3 Parasitology and Biomedicine Institute ‘Lopez Neyra’, CSIC, Granada, Spain and 4 Department of Biochemistry, Molecular Biology B and Immunology, University of Murcia, Murcia, Spain
*To whom correspondence should be addressed at Department of Biochemistry, Molecular Biology B and Immunology, Facultad de Medicina, Campus de Espinardo, Apartado de Correos 4021, Universidad de Murcia, 30100-Murcia, Spain. Tel: +34 968 369090; Fax: 34 968 369678; Email: jyelamos{at}um.es
Poly(ADP-ribose) polymerase-1 (PARP-1) has been involved in endothelial cell dysfunction associated with various pathophysiological conditions. The intrinsic mechanism of PARP-1-mediated endothelial cell dysfunction could be related to PARP-1 overactivation, NAD+ consumption and ATP depletion. An alternative way could involve transcription regulation. By using high-density microarrays, we examined early tumor necrosis factor 
(TNF-)-stimulated gene expression profiles in PARP-1+/+ and PARP-1–/– murine heart endothelial cells. TNF- modulated a significant number of genes in both cell types. We have identified a set of genes whose expression in response to TNF- is modulated by PARP-1, whereas the expression of others is PARP-1-independent. Up-regulation of several genes involved in the inflammatory response is hampered in the absence of PARP-1. Moreover, NF-
B-dependent transcriptional activation is partially inhibited in PARP-1–/– compared to PARP-1+/+ cells. However, we found that PARP-1 might also silence transcription of several NF-B target genes. Overall, our results show that PARP-1 is regulating the expression of genes by the endothelial cells both in a positive and a negative fashion, with the final effects depending on the gene. Individual studies of these genes are now necessary to clarify the intrinsic mechanism by which PARP-1 is controlling transcription and thereby finding out different therapeutic approaches involving PARP-1.
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