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G‐CSF contributes at the healing of tunica media of arteriotomy‐injured rat carotids by promoting differentiation of vascular smooth muscle cells
Author(s) -
Rinaldi Barbara,
Finicelli Mauro,
Donniacuo Maria,
Di Bernardo Giovanni,
Gritti Giulia,
Gaudio Stefania Del,
Forte Amalia,
Peluso Gianfranco,
Cipollaro Marilena,
Rossi Francesco,
Galderisi Umberto
Publication year - 2016
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.25074
Subject(s) - arteriotomy , tunica media , vascular smooth muscle , smooth muscle , medicine , wound healing , pathology , anatomy , microbiology and biotechnology , biology , artery , surgery
Restenosis is a complex pathophysiological disease whose causative mechanisms are not fully understood. Previous studies allowed us to demonstrate the efficacy of bone marrow mesenchymal stromal cells (MSCs) transplantation in limiting the pathophysiological remodeling in a model of arteriotomy‐induced (re) stenosis. In the current research we studied the effectiveness of G‐CSF treatment on male rate rats that were subjected carotid arteriotomy in order to evaluate a potentially effective non‐invasive strategy that recapitulates the MSC‐mediated recovery of injured vessels. WKY male rats were subjected carotid arteriotomy and given a nine day treatment (3 days pre‐ to 6 days post‐arteriotomy) with G‐CSF or saline. Carotids were harvested 7 and 30 days following arteriotomy (early‐ and late‐phase, respectively). Although morphometrical analysis did not reveal differences in lumen narrowing between G‐CSF‐ and PBS‐carotids 30 days following arteriotomy, we detected a noticeable conservative effect of G‐CSF treatment on vascular wall morphology. Histological and molecular analysis revealed an increase in cellularity within the tunica media with a concomitant increase of the VSMCs differentiation markers both at early‐ and late‐phases of (re) stenotic response in G‐CSF‐treated carotids (Sm22‐alpha, Myocd, and Smtn). These findings were accompanied by the downregulation of oxidative stress‐related genes in G‐CSF‐injured rats. The effect exerted by G‐CSF in our model of arteriotomy‐induced (re) stenosis seemed support the recovery of the architecture of the tunica media of injured vessels by: (i) inducing VSMCs differentiation; and (ii) limiting the oxidative‐stress response induced by arteriotomy. J. Cell. Physiol. 230: 215–223, 2016. © 2015 Wiley Periodicals, Inc.