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In Vivo Bioluminescence Imaging Reveals Redox-regulated AP-1 Activation in Paraventricular Nucleus of Mice with Renovascular Hypertension

Burmeister, Melissa A. ; Young, Colin N. ; Braga, Valdir A. ; Butler, Scott D. ; Sharma, Ram V. ; Davisson, Robin L.

Hypertension (Dallas, Tex. 1979), 2010-12, Vol.57 (2), p.289-297 [Periódico revisado por pares]

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  • Título:
    In Vivo Bioluminescence Imaging Reveals Redox-regulated AP-1 Activation in Paraventricular Nucleus of Mice with Renovascular Hypertension
  • Autor: Burmeister, Melissa A. ; Young, Colin N. ; Braga, Valdir A. ; Butler, Scott D. ; Sharma, Ram V. ; Davisson, Robin L.
  • É parte de: Hypertension (Dallas, Tex. 1979), 2010-12, Vol.57 (2), p.289-297
  • Descrição: Renovascular hypertension (RVH) in mice is characterized by an elevation in hypothalamic angiotensin-II (Ang-II) levels. The paraventricular nucleus (PVN) is a major cardioregulatory site implicated in the neurogenic component of RVH. Increased superoxide (O 2 −· ) production in the PVN is involved in Ang-II-dependent neuro-cardiovascular diseases such as hypertension and heart failure. Here we tested the hypothesis that excessive O 2 −· production and activation of the redox-regulated transcription factor activator protein-1 (AP-1) in PVN contributes to the development and maintenance of RVH. Male C57Bl/6 mice underwent implantation of radiotelemeters, bilateral PVN injections of an adenovirus (Ad) encoding superoxide dismutase (AdCuZnSOD) or a control gene (LacZ), and unilateral renal artery clipping (2K1C) or sham surgery. AP-1 activity was longitudinally monitored in vivo by bioluminescence imaging in 2K1C or sham mice that had undergone PVN-targeted microinjections of an Ad encoding the firefly luciferase (Luc) gene downstream of AP-1 response elements (AdAP-1Luc). 2K1C evoked chronic hypertension and an increase in O 2 −· production in the PVN. Viral delivery of CuZnSOD to the PVN not only prevented the elevation in O 2 −· , but also abolished RVH. 2K1C also caused a surge in AP-1 activity in the PVN, which paralleled the rise in O 2 −· production in this brain region, and this was prevented by treatment with AdCuZnSOD. Finally, Ad-mediated expression of a dominant-negative inhibitor of AP-1 activity in the PVN prevented 2K1C-evoked hypertension. These results implicate oxidant signaling and AP-1 transcriptional activity in the PVN as key mediators in the pathogenesis of RVH.
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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