Publication: Nestin and WT1 expression in atheromatous
plaque neovessels: association with vulnerability
Authors
Fittipaldi, Silvia ; Vasuri, Francesco ; Degiovann, Alessio ; Pini, Rodolfo ; Mauro, Raffaella ; Faggioli, Gianluca ; D'Errico-Grigioni, Antonia ; Stella, Andrea ; Pasquinelli, Gianandrea
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Publisher
F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
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DOI
https://doi.org/10.14670/HH-29.1565
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info:eu-repo/semantics/article
Description
Abstract
Introduction. Neoangiogenesis is crucial for
the progression and vulnerability of atheromasic lesions.
Since adult vasa vasorum, which represent the
neoangiogenetic burden of healthy arteries,
constitutively express Nestin and Wilms Tumor (WT1),
the aims of the present study are: i) to describe and
quantify Nestin and WT1 in plaque neovessels; ii) to
investigate the relationship between neovessel
phenotype and plaque instability.
Methods. We prospectively evaluated 49 consecutive
carotid endarterectomy specimens. Histopathological
characteristics were separately collected, particularly the
intraplaque histological complications. Immunohistochemistry was carried out for CD34, Nestin and WT1;
the density of positivity was evaluated for each marker.
RT-PCR was performed to assess Nestin and WT1
mRNA levels on the first 10 plaques and on 10 control
arteries.
Results. Six (12.2%) plaques showed no neoangiogenesis. In the others, the mean immunohistochemical densities of CD34, Nestin, and WT1-positive
structures were 41.88, 28.84 and 17.68/mm2. Among the
CD34+ neovessels, 68% and 42% expressed Nestin and
WT1 respectively, i.e., nearly 36% of the neovessels
resulted to be Nestin+/WT1-. Furthermore, complicated
plaques (n=30) showed significantly more CD34 and
Nestin-positive vessels than uncomplicated plaques
(n=13; P=0.045 and P=0.009), while WT1 was not
increased (P=0.139). RT-PCR confirmed that WT1 gene
expression was 3-fold lower than Nestin gene in plaques
(p=0.001).
Conclusions. Plaque neoangiogenesis shows both a
Nestin+/WT1- and a Nestin+/WT1+ phenotype. The
Nestin+/WT1- neovessels are significantly more
abundant in complicated (vulnerable) plaques. The
identification of new transcription factors in plaque
neoangiogenesis, and their possible regulation, can open
new perspectives in the therapy of vulnerable plaques.
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