Endothelial committed oral stem cells as modelling in the relationship between periodontal and cardiovascular disease. Issue 10 (30th March 2018)
- Record Type:
- Journal Article
- Title:
- Endothelial committed oral stem cells as modelling in the relationship between periodontal and cardiovascular disease. Issue 10 (30th March 2018)
- Main Title:
- Endothelial committed oral stem cells as modelling in the relationship between periodontal and cardiovascular disease
- Authors:
- Pizzicannella, Jacopo
Diomede, Francesca
Merciaro, Ilaria
Caputi, Sergio
Tartaro, Armando
Guarnieri, Simone
Trubiani, Oriana - Abstract:
- Abstract : In the present study we have mimicked, in vitro, an inflammatory process using Lipopolysaccharide derived from Porphyromonas Gingivalis (LPS‐G) and human Periodontal Ligament Stem Cells induced to endothelial differentiation (e‐hPDLSCs). The research project has been organized into the three following steps: i) induction of hPDLSCs toward endothelial differentiation; ii) evaluation of the molecular signaling pathway involved in the response to the LPS‐G, and iii) functional response evaluation of the living construct constituted by porcine decellularized valve/e‐hPDLSCs treated with LPS‐G. Obtained results showed that 5 μg/ml LPS‐G stimulus provokes: a slowdown of cell growth starting from 24 hr and the release of IL6, IL8, and MCP1 molecules. Signaling network analyzed showed the activation of TLR4/ NFkB/ERK1/2/p‐ERK1/2 signaling mediated by MyD88 in LPS‐G stimulated e‐hPDLSCs, moreover a time course put in evidence a nuclear traslocation of ERK1/2 and p‐ERK1/2 in differentiated samples. Following, the ability of e‐hPDLSCs to expand and colonize the decellularized porcine heart valves was appraised at ultrastructural level. Considering that, the Reactive Oxygen Species (ROS) play an important role in the progression and development of cardiovascular disease (CVD), in LPS‐G living construct model e‐hPDLSCs/decellularized porcine heart valves (dPHV), ROS production was assessed. Time lapse experiments evidenced that LPS‐G provokes in e‐hPDLSCs a rapid and sustainedAbstract : In the present study we have mimicked, in vitro, an inflammatory process using Lipopolysaccharide derived from Porphyromonas Gingivalis (LPS‐G) and human Periodontal Ligament Stem Cells induced to endothelial differentiation (e‐hPDLSCs). The research project has been organized into the three following steps: i) induction of hPDLSCs toward endothelial differentiation; ii) evaluation of the molecular signaling pathway involved in the response to the LPS‐G, and iii) functional response evaluation of the living construct constituted by porcine decellularized valve/e‐hPDLSCs treated with LPS‐G. Obtained results showed that 5 μg/ml LPS‐G stimulus provokes: a slowdown of cell growth starting from 24 hr and the release of IL6, IL8, and MCP1 molecules. Signaling network analyzed showed the activation of TLR4/ NFkB/ERK1/2/p‐ERK1/2 signaling mediated by MyD88 in LPS‐G stimulated e‐hPDLSCs, moreover a time course put in evidence a nuclear traslocation of ERK1/2 and p‐ERK1/2 in differentiated samples. Following, the ability of e‐hPDLSCs to expand and colonize the decellularized porcine heart valves was appraised at ultrastructural level. Considering that, the Reactive Oxygen Species (ROS) play an important role in the progression and development of cardiovascular disease (CVD), in LPS‐G living construct model e‐hPDLSCs/decellularized porcine heart valves (dPHV), ROS production was assessed. Time lapse experiments evidenced that LPS‐G provokes in e‐hPDLSCs a rapid and sustained increase in ROS generation, negligible on undifferentiated cells. From obtained data, by multiparametric analyses, a reasonable conclusion may be that the inflammation process activated by LPS‐G can affect endothelial cells and could represent in vivo a possible pathological and predictor state of CVD. Abstract : The research project has been organized into the three following steps: i) induction of hPDLSCs toward endothelial differentiation; ii) evaluation of the molecular signaling pathway involved in the response to the LPS‐G, and iii) functional response evaluation of the living construct constituted by porcine decellularized valve/e‐hPDLSCs treated with LPS‐G. From obtained data, by multiparametric analyses, a reasonable conclusion may be that the inflammation process activated by LPS‐G can affect endothelial cells and could represent in vivo a possible pathological and predictor state of CVD. … (more)
- Is Part Of:
- Journal of cellular physiology. Volume 233:Issue 10(2018:Oct.)
- Journal:
- Journal of cellular physiology
- Issue:
- Volume 233:Issue 10(2018:Oct.)
- Issue Display:
- Volume 233, Issue 10 (2018)
- Year:
- 2018
- Volume:
- 233
- Issue:
- 10
- Issue Sort Value:
- 2018-0233-0010-0000
- Page Start:
- 6734
- Page End:
- 6747
- Publication Date:
- 2018-03-30
- Subjects:
- cardiovascular disease -- endothelial differentiation -- human periodontal ligament stem cells -- LPS‐G -- periodontal disease
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.26515 ↗
- 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:
- 23016.xml