G‐CSF contributes at the healing of tunica media of arteriotomy‐injured rat carotids by promoting differentiation of vascular smooth muscle cells. Issue 1 (28th September 2015)
- Record Type:
- Journal Article
- Title:
- G‐CSF contributes at the healing of tunica media of arteriotomy‐injured rat carotids by promoting differentiation of vascular smooth muscle cells. Issue 1 (28th September 2015)
- Main Title:
- G‐CSF contributes at the healing of tunica media of arteriotomy‐injured rat carotids by promoting differentiation of vascular smooth muscle cells
- Authors:
- Rinaldi, Barbara
Finicelli, Mauro
Donniacuo, Maria
Di Bernardo, Giovanni
Gritti, Giulia
Gaudio, Stefania Del
Forte, Amalia
Peluso, Gianfranco
Cipollaro, Marilena
Rossi, Francesco
Galderisi, Umberto - Abstract:
- Abstract : 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 ofAbstract : 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. … (more)
- Is Part Of:
- Journal of cellular physiology. Volume 231:Issue 1(2016:Jan.)
- Journal:
- Journal of cellular physiology
- Issue:
- Volume 231:Issue 1(2016:Jan.)
- Issue Display:
- Volume 231, Issue 1 (2016)
- Year:
- 2016
- Volume:
- 231
- Issue:
- 1
- Issue Sort Value:
- 2016-0231-0001-0000
- Page Start:
- 215
- Page End:
- 223
- Publication Date:
- 2015-09-28
- Subjects:
- Physiology -- Periodicals
Cell physiology -- Periodicals
571.6 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1097-4652 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1002/jcp.25074 ↗
- Languages:
- English
- ISSNs:
- 0021-9541
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4955.020000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 15451.xml