scholarly journals Moderate Alcohol Consumption Targets S100β + Vascular Stem Cells and Attenuates Injury‐Induced Neointimal Hyperplasia

2020 ◽  
Vol 44 (9) ◽  
pp. 1734-1746
Author(s):  
Weimin Liu ◽  
Suzie Harman ◽  
Mariana DiLuca ◽  
Denise Burtenshaw ◽  
Eoin Corcoran ◽  
...  
2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Wen-Chin Huang ◽  
Aijun Wang ◽  
Song Li

Vascular disease, such as neointimal hyperplasia and atherosclerosis, involves in migration and proliferation of vascular cells in blood vessel wall. It is generally accepted that the de-differentiation of vascular smooth muscle cells (SMCs) contributes to vascular diseases. However, previous studies suggest that resident multipotent vascular stem cells (MVSCs) are also involved in neointima formation. In this study, we isolated MVSCs from the medial layer of human carotid artery and thoracic aorta by explant cultures, characterized these cells, and identified the origin of these vascular cells populated in lesion areas. Human MVSCs could be isolated from healthy and diseased blood vessels, were cloneable, and were positive for stem cell markers SOX10 and SOX17 but not SMC markers α-actin and calponin-1. MVSCs were able to differentiate into neural cells, SMCs and other mesenchymal lineages in vitro. In addition, we examined the location of MVSCs in diseased vascular wall by immunohistochemistry. The majority of cells within tunica media were calponin-positive cells, whereas a small population of cells was proliferative and double positive for SOX10 and Ki67 in the border between tunica intima and media. The number of SOX10+ cells in atherosclerotic lesions was more than that in healthy blood vessels, and some of these cells were double positive for SOX10 and chondrogenic markers. Furthermore, we performed in situ PCR and proximity ligation assays to stain for the epigenetic markers of SMC lineage. The results suggested that SOX10+ cells in cell cultures and tissue sections were not derived from de-differentiated SMCs. In conclusion, these findings support that MVSCs contributes to human vascular diseases.


2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Xiaohu Meng ◽  
Wenjie Su ◽  
Xuan Tao ◽  
Mingyang Sun ◽  
Rongchao Ying ◽  
...  

Atherosclerosis is considered as a multifactorial disease in terms of the pathogenic mechanisms. Oxidative stress has been implicated in atherogenesis, and the putative mechanisms of its action include oxidative modification of redox-sensitive signaling factors. High mobility group box 1 (HMGB1) is a key inflammatory mediator in atherosclerosis, but if oxidized it loses its activity. Thus, whether and how it participates in oxidative stress-induced atherosclerosis are not clear. The current study found that exogenous HMGB1 dose-dependently inhibited the proliferation of multipotent vascular stem cells and their differentiation to smooth muscle cells induced by platelet-derived growth factor. But oxidative modification impaired the activity of HMGB1 to produce the effect. The stem cells were regarded as the source of smooth muscle cells in vascular remodeling and neointimal hyperplasia. Therefore, the findings suggested that HMGB1 participated in oxidative stress-induced atherosclerosis presumably by targeting multipotent vascular stem cells.


1990 ◽  
Vol 63 (03) ◽  
pp. 345-348 ◽  
Author(s):  
J Veenastra ◽  
C Kluft ◽  
Th Ockhuizen ◽  
H v d Pol ◽  
M Wedel ◽  
...  

SummaryShort-term effects of moderate alcohol consumption on platelet function, tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) were studied in two age groups of volunteers (20–30 and 45–55 years), each consisting of eight healthy males. The alcohol (30 g in red port and wine) was consumed during a standard dinner. Two blood samples were drawn: one in the postprandial phase, and one the next morning after fasting overnight. Alcohol consumption tended to increase platelet aggregation and production of hydroxy fatty acids, reduced plasma t-PA activity and increased PAI activity in the postprandial phase. After the overnight fast the effects on t-PA and PAI had disappeared whereas at that time alcohol consumption tended to decrease platelet function. The effects of alcohol on t-PA and PAI activity appeared mainly in the older age group, whereas the t-PA activity in this group was already much lower, irrespective of alcohol consumption.


2016 ◽  
Vol 118 (1) ◽  
pp. 127-137 ◽  
Author(s):  
Sadie C. Slater ◽  
Michele Carrabba ◽  
Paolo Madeddu

2008 ◽  
Vol 68 (6) ◽  
pp. 988-995 ◽  
Author(s):  
Pierre Valeix ◽  
Patrice Faure ◽  
Sandrine Bertrais ◽  
Anne-Claire Vergnaud ◽  
Luc Dauchet ◽  
...  

2012 ◽  
Vol 28 (9) ◽  
pp. e492-e493
Author(s):  
Tomoyuki Matsumoto ◽  
Aki Osawa ◽  
Sheila Ingham ◽  
Alison Logar ◽  
Arvydas Usas ◽  
...  

2005 ◽  
Vol 352 (3) ◽  
pp. 245-253 ◽  
Author(s):  
Meir J. Stampfer ◽  
Jae Hee Kang ◽  
Jennifer Chen ◽  
Rebecca Cherry ◽  
Francine Grodstein

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