scholarly journals Protective Effect of Catalpol on Myocardium in Rats with Isoprenaline-Induced Myocardial Infarcts via Angiogenesis through Endothelial Progenitor Cells and Notch1 Signaling Pathway

2013 ◽  
Vol 04 (08) ◽  
pp. 619-627 ◽  
Author(s):  
Jing Zeng ◽  
Feng Huang ◽  
Yuangqing Tu ◽  
Saichun Wu ◽  
Manping Li ◽  
...  
Keyword(s):  
Protective Effect ◽  
Progenitor Cells ◽  
Signaling Pathway ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor ◽  
Notch1 Signaling ◽  
Notch1 Signaling Pathway

scholarly journals Platelet-Rich Plasma with Endothelial Progenitor Cells Accelerates Diabetic Wound Healing in Rats by Upregulating the Notch1 Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Cheng Zhang ◽  
Yu Zhu ◽  
Shengdi Lu ◽  
Wanrun Zhong ◽  
Yanmao Wang ◽  
...  
Keyword(s):  
Wound Healing ◽  
Growth Factors ◽  
Signaling Pathway ◽  
Platelet Rich Plasma ◽  
Diabetic Wound ◽  
Endothelial Progenitor ◽  
Notch1 Signaling ◽  
Diabetic Wound Healing ◽  
Notch1 Signaling Pathway ◽  
Diabetic Wounds

Diabetic wounds, as a kind of refractory wound, are very difficult to heal. Both endothelial progenitor cell (EPC) transplantation and platelet-rich plasma (PRP) can improve diabetic wound healing to some extent. However, PRP application cannot provide reparative cells, while EPC transplantation cannot replenish the required growth factors for wound healing. Thus, when applied alone, neither of these factors is sufficient for effective wound healing. Furthermore, the proliferation, differentiation, and fate of the transplanted EPCs are not well known. Therefore, in this study, we examined the efficacy of combined PRP application with EPC transplantation in diabetic wound healing. Our results indicated that PRP application improved EPC proliferation and migration. The Notch signaling pathway plays a key role in the regulation of the proliferation and differentiation of stem cells and angiogenesis in wound healing. The application of PRP upregulated the Notch pathway-related gene and protein expression in EPCs. Furthermore, experiments with shNotch1-transfected EPCs indicated that PRP enhanced the function of EPCs by upregulating the Notch1 signaling pathway. In vivo studies further indicated that the combination of PRP and EPC transplantation increased neovascularization, reduced wound size, and improved healing in rat wound models. Thus, PRP application can provide the necessary growth factors for wound healing, while EPC transplantation offers the required cells, indicating that the combination of both is a potent novel approach for treating diabetic wounds.

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

scholarly journals Enzyme-Aided Extraction of Fucoidan by AMG Augments the Functionality of EPCs through Regulation of the AKT/Rheb Signaling Pathway

Marine Drugs ◽  
2019 ◽  
Vol 17 (7) ◽  
pp. 392
Author(s):  
Vinoth Kumar Rethineswaran ◽  
Yeon-Ju Kim ◽  
Woong Bi Jang ◽  
Seung Taek Ji ◽  
Songhwa Kang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Wound Healing ◽  
Cell Migration ◽  
Progenitor Cells ◽  
Signaling Pathway ◽  
Endothelial Progenitor Cells ◽  
Bioactive Compounds ◽  
Tube Formation ◽  
Oxygen Species ◽  
Endothelial Progenitor

The purpose of the present study is to improve the endothelial progenitor cells (EPC) activation, proliferation, and angiogenesis using enzyme-aided extraction of fucoidan by amyloglucosidase (EAEF-AMG). Enzyme-aided extraction of fucoidan by AMG (EAEF-AMG) significantly increased EPC proliferation by reducing the reactive oxygen species (ROS) and decreasing apoptosis. Notably, EAEF-AMG treated EPCs repressed the colocalization of TSC2/LAMP1 and promoted perinuclear localization of mTOR/LAMP1 and mTOR/Rheb. Moreover, EAEF-AMG enhanced EPC functionalities, including tube formation, cell migration, and wound healing via regulation of AKT/Rheb signaling. Our data provided cell priming protocols to enhance therapeutic applications of EPCs using bioactive compounds for the treatment of CVD.

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.

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