scholarly journals Erratum. Adiponectin Prevents Diabetic Premature Senescence of Endothelial Progenitor Cells and Promotes Endothelial Repair by Suppressing the p38 MAP Kinase/p16 INK4A Signaling Pathway. Diabetes 2010;59:2949–2959

Diabetes ◽  
2016 ◽  
Vol 65 (10) ◽  
pp. 3219.1-3219 ◽  
Author(s):  
Junlei Chang ◽  
Yiming Li ◽  
Yu Huang ◽  
Karen S.L. Lam ◽  
Ruby L.C. Hoo ◽  
...  
Keyword(s):  
Map Kinase ◽  
Progenitor Cells ◽  
Signaling Pathway ◽  
Endothelial Progenitor Cells ◽  
P38 Map Kinase ◽  
Premature Senescence ◽  
Endothelial Progenitor ◽  
Endothelial Repair ◽  
P16 Ink4a

scholarly journals Reduced Circulating Endothelial Progenitor Cells and Downregulated GTCPH I Pathway Related to Endothelial Dysfunction in Premenopausal Women with Isolated Impaired Glucose Tolerance

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Juan Liu ◽  
Xiangbin Xing ◽  
Xinlin Wu ◽  
Xiang Li ◽  
Shun Yao ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Progenitor Cells ◽  
Signaling Pathway ◽  
Endothelial Progenitor Cells ◽  
Premenopausal Women ◽  
Endothelial Progenitor ◽  
Repair Capacity ◽  
Circulating Endothelial Progenitor Cells ◽  
Endothelial Repair

Background. Individuals at a prediabetic stage have had an augmented cardiovascular disease (CVD) risk and CVD-related mortality compared to normal glucose tolerance (NGT) individuals, which may be attributed to the impaired vascular endothelial repair capacity. In this study, circulating endothelial progenitor cells’ (EPCs) number and activity were evaluated, and the underlying mechanisms in premenopausal women with impaired glucose regulation were explored. Methods. Circulating EPCs’ number and activity and flow-mediated dilation (FMD) were compared in premenopausal women with NGT, isolated impaired fasting glucose (i-IFG), or isolated impaired glucose tolerance (i-IGT). Plasma nitric oxide (NO), EPCs-secreted NO, and intracellular BH4 levels were also measured. The key proteins (Tie2, Akt, eNOS, and GTPCH I) in the guanosine triphosphate cyclohydrolase/tetrahydrobiopterin (GTPCH/BH4) pathway and Tie2/Akt/eNOS signaling pathway were evaluated in these women. Results. It was observed that the i-IGT premenopausal women not i-IFG premenopausal women had a significant reduction in circulating EPCs’ number and activity as well as reduced FMD when compared to NGT subjects. Plasma NO levels or EPCs-secreted NO also decreased only in i-IGT women. The expression of GTCPH I as well as intracellular BH4 levels declined in i-IGT women; however, the alternations of key proteins’ expression in the Tie2/Akt/eNOS signaling pathway were not observed in either i-IGT or i-IFG women. Conclusions. The endothelial repair capacity was impaired in i-IGT premenopausal women but was preserved in i-IFG counterparts. The underlying mechanism may be associated with the downregulated GTCPH I pathway and reduced NO productions.

scholarly journals Hypoxic Preconditioning Enhances Biological Function of Endothelial Progenitor Cells via Notch-Jagged1 Signaling Pathway

2017 ◽  
Vol 23 ◽  
pp. 4665-4667 ◽  
Author(s):  
Qian Wang ◽  
LiHua Liu ◽  
YuanYuan Li ◽  
Jinfeng Wang ◽  
Yun Liu ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Signaling Pathway ◽  
Endothelial Progenitor Cells ◽  
Biological Function ◽  
Hypoxic Preconditioning ◽  
Endothelial Progenitor

scholarly journals Decreased Count and Dysfunction of Circulating EPCs in Postmenopausal Hypercholesterolemic Females via Reducing NO Production

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Ying Luo ◽  
Quan-Neng Yan ◽  
Wan-Zhou Wu ◽  
Fan-Yan Luo
Keyword(s):  
Endothelial Dysfunction ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Therapeutic Strategy ◽  
No Production ◽  
Endothelial Progenitor ◽  
Endothelial Repair ◽  
Flow Mediated Dilatation ◽  
Premenopausal Female ◽  
And Function

Endothelial progenitor cells (EPCs) contribute to the endogenous endothelial repair program during hypercholesterolemia. EPC count and migratory and proliferative capacities remain unchanged in the premenopausal female with hypercholesterolemia. However, the changes of count and activity of circulating EPCs in the hypercholesterolemic postmenopausal females are unknown. Here, we find that the migratory and proliferative capacities of circulating EPCs were decreased in patients with hypercholesterolemia versus normocholesterolemia. No significant differences were found between postmenopausal females and age-matched males. NO production showed positive correlation with the activity and count of circulating EPCs in patients with hypercholesterolemia. Flow-mediated dilatation (FMD) is directly interrelated with EPC counts and function. Our findings reveal that decreased EPC count and endothelial dysfunction lead to less NO production in hypercholesterolemic postmenopausal females. Maintaining the EPC numbers and activity might be emerging as a potential therapeutic strategy to reduce the risk of cardiovascular injury in elder women.

scholarly journals Impaired Endothelial Repair Capacity of Early Endothelial Progenitor Cells in Prehypertension

Hypertension ◽  
2010 ◽  
Vol 55 (6) ◽  
pp. 1389-1397 ◽  
Author(s):  
Giovanna Giannotti ◽  
Carola Doerries ◽  
Pavani S. Mocharla ◽  
Maja F. Mueller ◽  
Ferdinand H. Bahlmann ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor ◽  
Repair Capacity ◽  
Endothelial Repair

scholarly journals Elevated GTP Cyclohydrolase I Pathway in Endothelial Progenitor Cells of Overweight Premenopausal Women

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Shaohong Wu ◽  
Hao He ◽  
Ge-Xiu Liu ◽  
Xiao-Peng Li ◽  
Shun Yao ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Premenopausal Women ◽  
Normal Weight ◽  
Female Group ◽  
No Production ◽  
Endothelial Progenitor ◽  
Endothelial Repair ◽  
Significant Difference

Background/Aims. Sexual differences exist in endothelial progenitor cells (EPCs), and various cardiovascular risk factors are associated with the preservation of endothelial function in premenopausal women. However, it is unclear whether differences in endothelial function and circulating EPCs exist between overweight premenopausal women and age-matched men. Methods. We compared EPC counting and functions in normal-weight and overweight premenopausal women and men, evaluated endothelial function in each group, and detected the expression of the guanosine triphosphate cyclohydrolase I (GTPCH I) pathway. Results. The number of EPCs was lower in the male group than in the female group, regardless of normal-weight or overweight status, and there was no significant difference between the different weight groups among females or males. Endothelial function and EPC migration and proliferation were preserved in overweight premenopausal women compared with overweight men as were nitric oxide (NO) levels in plasma and secreted by EPCs. Endothelial function, the circulating EPC population, and NO levels were not different between normal-weight and overweight premenopausal women. Flow-mediated dilatation was significantly correlated with EPC function, plasma NO levels, and EPC-secreted NO. Conclusions. This investigation provides the first evidence for sex-based differences in EPC activity and endothelial function in overweight middle-aged individuals; these differences are associated with alterations in NO production and may partly occur through downregulation of the GTPCH I pathway. The present results provide new insights into the mechanism underlying the preserved endothelial function in overweight premenopausal women and may uncover a potential therapeutic target for endothelial repair in overweight population.

Endothelial progenitor cells proliferated via MEK-dependent p42 MAPK signaling pathway

2014 ◽  
Vol 400 (1-2) ◽  
pp. 201-206 ◽  
Author(s):  
Ferry Sandra ◽  
Yudi Her Oktaviono ◽  
Mohammad Aris Widodo ◽  
Yanni Dirgantara ◽  
Angliana Chouw ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Signaling Pathway ◽  
Endothelial Progenitor Cells ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Endothelial Progenitor
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