NAMPT regulates senescence, proliferation, and migration of endothelial progenitor cells through the SIRT1 AS lncRNA/miR-22/SIRT1 pathway

2016 ◽  
Vol 478 (3) ◽  
pp. 1382-1388 ◽  
Author(s):  
Guang-feng Ming ◽  
Kai Wu ◽  
Kai Hu ◽  
Yao Chen ◽  
Jian Xiao
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Protective Effect of Silymarin against Rapamycin-induced Apoptosis and Proliferation Inhibition in Endothelial Progenitor Cells

2015 ◽  
Vol 10 (2) ◽  
pp. 1934578X1501000 ◽  
Author(s):  
Peng Zhang ◽  
Guohua Han ◽  
Pei Gao ◽  
Kun Qiao ◽  
Yusheng Ren ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Mononuclear Cells ◽  
Control Group ◽  
Dependent Manner ◽  
Endothelial Progenitor ◽  
Concentration Dependent Manner ◽  
Inhibition Of Proliferation ◽  
And Migration ◽  
Proliferation And Migration

For this study, peripheral blood samples were collected from human volunteers. Mononuclear cells (MNC) were separated by density centrifugation and were induced to differentiate into endothelial progenitor cells (EPCs) in vitro. Different concentrations of rapamycin and silymarin were introduced to the EPCs over 24 hours and then EPCs were analyzed for proliferation, migration, apoptosis and angiogenesis. Compared with the control group, rapamycin (1, 10, 100 ng/mL) inhibited the proliferation and migration of EPCs in a concentration dependent manner ( P<0.05). Silymarin (50, 100 μg/mL) enhanced the proliferation and migration of EPCs and inhibited apoptosis in a concentration dependent manner ( P<0.05). By adding rapamycin (1 ng/mL) and silymarin (25, 50, 100 μg/mL) over 24 hours, silymarin inhibited the pro-apoptotic effect of rapamycin on EPCs, and reversed the inhibition of proliferation, migration and angiogenesis of EPCs by rapamycin ( P<0.05).

scholarly journals Preliminary Study: Purple Sweet Potato Extract Seems to Be Superior to Increase the Migration of Impaired Endothelial Progenitor Cells Compared to l-Ascorbic Acid

2019 ◽  
Vol 87 (3) ◽  
pp. 16
Author(s):  
Yudi Her Oktaviono ◽  
Makhyan Jibril Al-Farabi ◽  
Luh Oliva Saraswati Suastika ◽  
Febriyanti Hartono ◽  
Yanni Dirgantara ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Sweet Potato ◽  
Acid Treatment ◽  
Endothelial Progenitor ◽  
Treatment Dose ◽  
Purple Sweet Potato ◽  
And Migration ◽  
Proliferation And Migration

Impairment of the endothelial progenitor cells (EPCs) ability to proliferate and migrate in the patients with coronary heart disease (CHD) is partly caused by oxidative stress. This research evaluates the effect of treatment with Ipomoea batatas L./purple sweet potato (PSP) extract and l-ascorbic acid on the proliferation and migration of impaired EPCs. EPCs were isolated from CHD patient’s peripheral blood. EPCs culture were cultivated and divided into control (untreated), PSP extract treatment (dose 1 and 25 μg/mL), and l-ascorbic acid treatment (dose 10 and 250 μg/mL) groups for 48 h. EPCs proliferation was analyzed with the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cell proliferation assay, and migration was evaluated with the cell migration assay kit. Statistical tests were evaluated using SPSS 25.0. This research showed that EPCs proliferation and migration was significantly higher in all PSP extract and l-ascorbic acid treatment compared to the control (p < 0.001). EPCs migration on treatment with a PSP extract dose of 25 μg/mL was significantly higher compared to the treatment with l-ascorbic acid dose of 250 μg/mL (303,000 ± 1000 compared to 215,000 ± 3000 cells, p< 0.001). In conclusion, both treatments with PSP extract and l-ascorbic acid can improve the proliferation and migration of impaired EPCs. At the dose of 25 μg/mL, PSP extract seems to be superior to the l-ascorbic acid dose of 250 μg/mL to improve EPCs migration.

scholarly journals Exosomes secreted from osteocalcin-overexpressing endothelial progenitor cells promote endothelial cell angiogenesis

2019 ◽  
Vol 317 (5) ◽  
pp. C932-C941 ◽  
Author(s):  
Ming Yi ◽  
Ye Wu ◽  
Jun Long ◽  
Fei Liu ◽  
Zhi Liu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Rat Aorta ◽  
Tube Formation ◽  
Endothelial Progenitor ◽  
And Migration ◽  
G Protein Coupled ◽  
Receptor Family ◽  
Proliferation And Migration

Exosome secretion is an important paracrine way of endothelial progenitor cells (EPCs) to modulate resident endothelial cells. The osteocalcin (OCN)-expressing EPCs have been found to be increased in cardiovascular disease patients and are considered to be involved in the process of coronary atherosclerosis. Since OCN has been proven to prevent endothelial dysfunction, this study aimed to evaluate the effect of exosomes derived from OCN-overexpressed EPCs on endothelial cells. Exosomes derived from EPCs (Exos) and OCN-overexpressed EPCs (OCN-Exos) were isolated and incubated with rat aorta endothelial cells (RAOECs) with or without the inhibition of OCN receptor G protein-coupled receptor family C group 6 member A (GPRC6A). The effects of exosomes on the proliferation activity of endothelial cells were evaluated by CCK-8 assay, and the migration of endothelial cells was detected by wound healing assay. A tube formation assay was used to test the influence of exosomes on the angiogenesis performance of endothelial cells. Here, we presented that OCN was packed into Exos and was able to be transferred to the RAOECs via exosome incorporation, which was increased in OCN-Exos groups. Compared with Exos, OCN-Exos had better efficiency in promoting RAOEC proliferation and migration and tube formation. The promoting effects were impeded after the inhibition of GPRC6A expression in RAOECs. These data suggest that exosomes from OCN-overexpressed EPCs have a beneficial regulating effect on endothelial cells, which involved enhanced OCN-GPRC6A signaling.

scholarly journals Reduced Number and Activity of Circulating Endothelial Progenitor Cells in Acute Aortic Dissection and Its Relationship With IL-6 and IL-17

2021 ◽  
Vol 8 ◽  
Author(s):  
Zhenhua Huang ◽  
Zhihao Liu ◽  
Keke Wang ◽  
Zi Ye ◽  
Yan Xiong ◽  
...  
Keyword(s):  
Aortic Dissection ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Acute Aortic Dissection ◽  
Inflammatory Factors ◽  
Interleukin 17 ◽  
Endothelial Progenitor ◽  
Circulating Endothelial Progenitor Cells ◽  
And Migration ◽  
Proliferation And Migration

This study investigates the alteration in function and number of circulating endothelial progenitor cells (EPCs) in patients with aortic dissection (AD), compared with hypertensive patients, and its possible mechanism. Thirty-four patients with acute aortic dissection (AAD) and 20 patients with primary hypertension were involved. Flow cytometry analysis was performed to detect the number of CD34+/KDR+ cells, and acetylated low density lipoprotein (ac-LDL) and lectin fluorescent staining method was applied to test the number of cultured EPCs. In addition, EPC migration and proliferation were measured, and plasma interleukin 6 (IL-6) and interleukin 17 (IL-17) levels were investigated. The number of circulating EPCs in the AAD group was lower than that in the non-AD group, and the proliferation and migration of circulating EPCs in the AAD group were lower than that in the non-AD group. In addition, the number, proliferation, and migration of circulating EPCs were significantly inversely correlated with the aortic dissection detection risk score (ADD-RS). More importantly, increased plasma IL-6 and IL-17 level was found in the AAD group, and the two inflammatory factors were inversely associated with the function and number of circulating EPCs in the AAD group. We first demonstrated that the number and function of circulating EPCs are reduced in the AAD group, which may be partly related to upregulated plasma IL-6 and IL-17. Our study provides novel insight on the underlying mechanism and potential therapeutic target of AAD.

scholarly journals Up-regulation of Grb2-associated binder 1 promotes hepatocyte growth factor-induced endothelial progenitor cell proliferation and migration

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6675
Author(s):  
Qing Fan ◽  
Liyu Zhang ◽  
Wenjie Zhu ◽  
Sheng Xue ◽  
Yisheng Song ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Adaptor Protein ◽  
Human Umbilical Cord ◽  
Endothelial Progenitor ◽  
And Migration ◽  
Hepatocyte Growth ◽  
Proliferation And Migration

Objectives Grb2-associated binder 1 (Gab1), a scaffolding adaptor protein, plays an important role in transmitting key signals that control cell growth, migration, and function from multiple tyrosine kinase receptors. This study was designed to investigate the influence of upregulation of Gab1 in endothelial progenitor cells (EPCs) stimulated with hepatocyte growth factor (HGF), and the underlying molecular mechanisms. Materials and Methods Endothelial progenitor cells isolated from human umbilical cord blood were identified and divided into four groups. EPCs in the Control group were cultured normally; those in the Control+HGF group were treated with HGF stimulation; those in the AD-Gab1 group were transfected with adenovirus containing the Gab1 gene but not treated with HGF stimulation; and, those in the AD-Gab1+HGF group were treated with both HGF stimulation and transfection with adenovirus containing the Gab1 gene. Subsequently, Gab1 expression and proliferation and migration ability were compared for EPCs grown under different conditions. Furthermore, we measured phosphorylation levels of three key proteins Gab1, SHP2, and ERK1/2. Results The AD-Gab1+HGF group had the highest expression of Gab1 and higher proliferation and migration than the other three groups. Conclusions Upregulation of Gab1 promoted HGF-induced EPC proliferation and migration. Mechanistically, HGF stimulated Gab1 tyrosine phosphorylation in EPCs, thus leading to activation of extracellular regulated MAP kinase 1/2, which is involved in proliferation and migration signaling.

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