http://www.cnr.it/ontology/cnr/individuo/prodotto/ID98964
Nitric Oxide is Required for Estrogen Regulation of hTERT Expression and Telomerase Activity in Human Endothelial Cells. (Abstract in rivista)
- Type
- Label
- Nitric Oxide is Required for Estrogen Regulation of hTERT Expression and Telomerase Activity in Human Endothelial Cells. (Abstract in rivista) (literal)
- Anno
- 2006-01-01T00:00:00+01:00 (literal)
- Alternative label
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Annalisa Grasselli1; Simona Nanni1; Claudia Colussi2; Ada Sacchi3; Carlo Gaetano4; Alfredo Pontecorvi5; Maurizio C Capogrossi6; Antonella Farsetti7 (literal)
- Pagina inizio
- Pagina fine
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#altreInformazioni
- Convegno
- American Heart Association (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#citta
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note
- Supplement to Circulation, 114 (18), Abstract N. 1396, 2006
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- 1 Istituto Regina Elena, Roma, Italy
2 Istituto Dermopatico dell' Immacolata, Roma, Italy
3 Istituto Regina Elena, Roma, Italy
4 Istituto Dermopatico dell' Immacolata, Roma, Italy
5 Università Cattolica del Sacro Cuore, Roma, Italy
6 Istituto Dermopatico dell' Immacolata, Roma, Italy
7 Istituto Neurobiologia & Medicina Molecolare-CNR, Roma, Italy (literal)
- Titolo
- Nitric Oxide is Required for Estrogen Regulation of hTERT Expression and Telomerase Activity in Human Endothelial Cells. (literal)
- Abstract
- INTRODUCTION & BACKGROUND: We have previously reported that nitric oxide (NO) is required for the VEGF-dependent angiogenic response and telomerase activity in human umbilical endothelial cells (HUVEC). In this study, we investigated the role of NO as a potential regulator of the estrogen (E2) responsiveness of the catalytic subunit of human telomerase (hTERT), a non traditional target of the estrogen receptor signaling.
METHODS & RESULTS: Upon E2 stimulation, HUVEC showed a significant induction of telomerase activity evaluated by TRAP assay which was paralleled by a prompt stimulation of hTERT mRNA expression. This effect was prevented by the NOS inhibitor 7-nitroindazole (7N). In the presence of E2, gel retardation (EMSA) and chromatin immunoprecipitation (ChIP) assays clearly showed a specific recruitment of both ERa and ERb onto the hTERT promoter as the result of intrinsic estrogen-dependent chromatin remodeling. This effect was abrogated in the presence of the estrogen antagonist ICI. To determine the specific role of eNOS in the estrogen-dependent activation of hTERT promoter, bovine aortic endothelial cells (BAEC) were transiently transfected with the constitutively active eNOS mutant S1177D in the presence of E2 and/or 7N. Remarkably,, the eNOS inhibitor abolished E2 and NO responsiveness of hTERT promoter. To directly address the role of NO in the E2-dependent regulation of hTERT, pulmonary endothelial cells (PEC) were isolated from eNOS-/- mice and grown in absence or presence of E2. In this condition, E2 significantly increased telomerase activity in wild-type cells whereas eNOS-/- cells exhibited a barely detectable telomerase activity that was not rescued upon E2 treatment.
CONCLUSIONS: Our results provide novel evidences leading to a molecular dissection of the NO contribution to the estrogen-dependent regulation of hTERT and telomerase activity in endothelial cells. (literal)
- Prodotto di
- Autore CNR
Incoming links:
- Autore CNR di
- Prodotto
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi
