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Injury to rat carotid arteries causes time-dependent changes in gene expression in contralateral uninjured arteries

Författare

  • Amalia Forte
  • Mauro Finicelli
  • Pasquale De Luca
  • Ina Nordström
  • Francesco Onorati
  • Cesare Quarto
  • Pasquale Sante
  • Attilio Renzulli
  • Umberto Galderisi
  • Liberato Berrino
  • Marisa De Feo
  • Per Hellstrand
  • Francesco Rossi
  • Maurizio Cotrufo
  • Antonino Cascino
  • Marilena Cipollaro

Summary, in English

Vascular surgery aimed at stenosis removal induces local reactions often leading to restenosis. Although extensive analysis has been focused on pathways activated in injured arteries, little attention has been devoted to associated systemic vascular reactions. The aim of the present study was to analyse changes occurring in contralateral uninjured rat carotid arteries in the acute phase following unilateral injury. WKY (Wistar-Kyoto) rats were subjected to unilateral carotid arteriotomy. Contralateral uninjured carotid arteries were harvested from 4 h to 7 days after injury. Carotid arteries were also harvested from sham-operated rats and uninjured rats. Carotid morphology and morphometry were examined. Affymetrix microarrays were used for differential analysis of gene expression. A subset of data was validated by real-time RT-PCR (reverse transcription-PCR) and verified at the protein level by Western blotting. A total of 1011 genes were differentially regulated in contralateral uninjured carotid arteries from 4 h to 7 days after arteriotomy (P < 0.0001; fold change, >= 2) and were classified into 19 gene ontology functional categories. To a lesser extent, mRNA variations also occurred in carotid arteries of sham-operated rats. Among the changes, up-regulation of members of the RAS (renin-angiotensin system) was detected, with possible implications for vasocompensative mechanisms induced by arteriotomy. In particular, a selective increase in the 69 kDa isoform of the N-domain of ACE (angiotensin-converting enzyme), and not the classical somatic 195 kDa isoform, was observed in contralateral uninjured carotid arteries, suggesting that this 69 kDa isoenzyme could influence local Angll (angiotensin II) production. In conclusion, systemic reactions to injury occur in the vasculature, with potential clinical relevance, and suggest that caution is needed in the choice of controls during experimental design in vivo.

Avdelning/ar

Publiceringsår

2009

Språk

Engelska

Sidor

125-136

Publikation/Tidskrift/Serie

Clinical Science

Volym

116

Issue

1-2

Dokumenttyp

Artikel i tidskrift

Förlag

Portland Press

Ämne

  • Physiology

Nyckelord

  • renin-angiotensin
  • remodelling
  • microarray
  • blood flow
  • inflammation
  • system
  • vascular injury

Status

Published

Forskningsgrupp

  • Vascular Physiology

ISBN/ISSN/Övrigt

  • ISSN: 1470-8736