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Cardiovascular Research 2003 60(3):654-663; doi:10.1016/j.cardiores.2003.08.015
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Stenosis progression after surgical injury in Milan hypertensive rat carotid arteries

Amalia Forte*,a, Salvatore Espositob, Marisa De Feoc, Umberto Galderisia, Cesare Quartoc, Ferdinando Espositoa, Attilio Renzullid, Liberato Berrinoa, Marilena Cipollaroa, Lucio Agozzinob, Maurizio Cotrufoc, Francesco Rossia and Antonino Cascinoa

aExcellence Research Center for Cardiovascular Diseases, Department of Experimental Medicine, Section of Biotechnology and Molecular Biology, Second University of Naples, Via Costantinopoli, 16, 80138 Naples, Italy
bDepartment of Public Medicine, Second University of Naples, Naples, Italy
cDepartment of Cardiothoracic Sciences, Second University of Naples, Naples, Italy
dUnit of Cardiac Surgery, University Magna Graecia, Catanzaro, Italy

*Corresponding author. Department of Experimental Medicine, Section of Biotechnology and Molecular Biology, Second University of Naples, Via Costantinopoli, 16, 80138 Naples, Italy. Tel.: +39-81-5665879; fax: +39-81-5667547. Email address: amalia.forte{at}unina2.it

Background: Milan hypertensive rats (MHS) are characterised by an increase in renal sodium reabsorption mainly related to adducin mutations. Interest in this model relies on the genetic link between adducin polymorphisms and primary hypertension, observed also in a subset of patients. Objectives: To investigate the molecular and morphological events involved in carotid stenosis and triggered by surgery in MHS model. Methods: Stenosis was induced through arteriotomy. At different times after injury, the expression profiles of various gene families were investigated by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR), while histological techniques were used to follow morphometric and morphological changes. Apoptotic nuclei were revealed by terminal deoxynucleotidyl transferase-dUTP nick end labelling (TUNEL). Results: mRNAs coding for transcription factors c-jun, c-fos and c-myc were rapidly induced by injury. Analysis of apoptosis-related genes revealed a decrease of the Bcl-2/Bax ratio 4 h after vascular trauma (P<0.05), followed by a recovery of antiapoptotic factors 24 and 48 h later. ETA and receptor mRNAs decreased after the injury and were replaced by ETB and AT2 mRNAs. Both ETA and AT1 turned to basal level 48 h after injury. Expression profiles of chatepsins B and D were also determined. A marked neoadventitia led to maximal 60±9% lumen reduction (P<0.05) 30 days after surgery. Media substitution by fibrotic and granulomatous tissue was also evident. Maximal 47±2% apoptotic nuclei were detected 48 h after the injury (P<0.05). Conclusions: The injury applied to MHS carotids induces negative remodelling and a limited apoptotic reaction. These findings could arise from the balancing among proliferative factors, apoptosis-related molecules and relaxant anti-proliferative receptors, all stimulated by the injury.

KEYWORDS Apoptosis; Remodelling; Hypertension; Gene expression; Restenosis; Vascular injury

Time for primary review 27 days


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