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Updated: Jul 4, 2026
Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery
Published on: December 23, 2014
Injury to rat carotid arteries causes time-dependent changes in gene expression in contralateral uninjured arteries
Amalia Forte1, Mauro Finicelli, Pasquale De Luca
1Excellence Research Centre for Cardiovascular Diseases, Department of Experimental Medicine, Second University of Naples, 80138 Naples, Italy. amalia.forte@unina2.it
Abstract:
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, >or=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 AngII (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.
Insights
Unilateral carotid artery injury triggers systemic vascular reactions in the contralateral uninjured artery. This study reveals gene expression changes and renin-angiotensin system activation, impacting experimental design.
Area of Science:
- Cardiovascular Biology
- Vascular Biology
- Molecular Medicine
Background:
- Vascular surgery for stenosis can cause restenosis.
- Focus has been on local arterial injury responses, neglecting systemic effects.
- Systemic vascular reactions following unilateral injury require investigation.
Purpose of the Study:
- To analyze changes in contralateral uninjured rat carotid arteries post-unilateral injury.
- To identify acute-phase systemic vascular reactions.
- To assess the impact on experimental controls.
Main Methods:
- Unilateral carotid arteriotomy in WKY rats.
- Gene expression profiling using Affymetrix microarrays.
- Validation via RT-PCR and Western blotting.
Main Results:
- 1011 genes were differentially regulated in contralateral arteries (4h-7d post-injury).
- Renin-angiotensin system (RAS) members were upregulated.
- A specific 69 kDa ACE isoform increased, suggesting AngII modulation.
Conclusions:
- Systemic vascular reactions occur following localized arterial injury.
- These reactions have potential clinical relevance.
- Careful consideration of controls is crucial in in vivo experimental designs.
