scholarly journals Role of Atorvastatin on Endothelial Cells and Endothelial Progenitor Cells in Cardiovascular Disease

2016 ◽  
pp. 151-154
Author(s):  
Sampath Kumar ◽  
Sujeetha Purushothaman ◽  
Papitha Ponnaiya ◽  
Keerthi Kishor ◽  
Vijaya Anand
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor

scholarly journals CHIR99021 Augmented the Function of Late Endothelial Progenitor Cells by Preventing Replicative Senescence

2021 ◽  
Vol 22 (9) ◽  
pp. 4796
Author(s):  
Vinoth Kumar Rethineswaran ◽  
Da Yeon Kim ◽  
Yeon-Ju Kim ◽  
WoongBi Jang ◽  
Seung Taek Ji ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Blood Circulation ◽  
Functional Role ◽  
Replicative Senescence ◽  
Endothelial Progenitor ◽  
Vascular Structures ◽  
Gsk 3Β

Endothelial progenitor cells (EPCs) are specialized cells in circulating blood, well known for their ability to form new vascular structures. Aging and various ailments such as diabetes, atherosclerosis and cardiovascular disease make EPCs vulnerable to decreasing in number, which affects their migration, proliferation and angiogenesis. Myocardial ischemia is also linked to a reduced number of EPCs and their endothelial functional role, which hinders proper blood circulation to the myocardium. The current study shows that an aminopyrimidine derivative compound (CHIR99021) induces the inhibition of GSK-3β in cultured late EPCs. GSK-3β inhibition subsequently inhibits mTOR by blocking the phosphorylation of TSC2 and lysosomal localization of mTOR. Furthermore, suppression of GSK-3β activity considerably increased lysosomal activation and autophagy. The activation of lysosomes and autophagy by GSK-3β inhibition not only prevented replicative senescence of the late EPCs but also directed their migration, proliferation and angiogenesis. To conclude, our results demonstrate that lysosome activation and autophagy play a crucial role in blocking the replicative senescence of EPCs and in increasing their endothelial function. Thus, the findings provide an insight towards the treatment of ischemia-associated cardiovascular diseases based on the role of late EPCs.

scholarly journals Effects of Brain-Derived Neurotrophic Factor on MicroRNA Expression Profile in Human Endothelial Progenitor Cells

2018 ◽  
Vol 27 (6) ◽  
pp. 1005-1009 ◽  
Author(s):  
Tongrong He ◽  
Ruohan Sun ◽  
Ying Li ◽  
Zvonimir S. Katusic
Keyword(s):  
Endothelial Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Endothelial Progenitor ◽  
Regenerative Capacity ◽  
Proliferation And Differentiation ◽  
Guanylate Binding Protein

The mechanisms underlying proangiogenic function of brain-derived neurotrophic factor (BDNF) are not fully understood. The current study was designed to explore the microRNA (miRNA) profile in human early endothelial progenitor cells (EPCs, also referred to as CFU-Hill cells) treated with BDNF. Treatment of early EPCs with BDNF for 7 d significantly increased the colony formation of outgrowth endothelial cells. BDNF suppressed the expression of miR-4716-5p, miR-3928, miR-433, miR-1294, miR-1539, and miR-19b-1*. In contrast, BDNF significantly increased the levels of miR-432*, miR-4499, miR-3911, miR-1183, miR-4669, miR-636, miR-4717-3p, miR-4298, miR485-5p, and miR-181c. Since miR-433 has been reported to augment hematopoietic cells proliferation and differentiation, we examined the role of miR-433 in regenerative effects of BDNF. BDNF stimulated the protein expression of guanylate-binding protein 2 via the suppression of miR-433. However, the knockdown of miR-433 was not sufficient to significantly increase the number of outgrowth endothelial cell colonies, suggesting that modulation of miR-433 alone does not stimulate regenerative capacity of EPCs. In aggregate, our results also suggest that the effect of BDNF on regenerative function of EPCs may depend on complex changes in the expression of microRNAs.

Endothelial progenitor cells in coronary artery disease

2013 ◽  
Vol 394 (10) ◽  
pp. 1241-1252 ◽  
Author(s):  
Michael Donahue ◽  
Cristina Quintavalle ◽  
Giovanni Alfonso Chiariello ◽  
Gerolama Condorelli ◽  
Carlo Briguori
Keyword(s):  
Cardiovascular Disease ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Prognostic Factor ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Vascular Health ◽  
Endothelial Progenitor ◽  
Artery Disease

Abstract In the last two decades a great deal of evidence has been collected on the key role of endothelial progenitor cells (EPC) in the mechanisms of vascular healing. The role of EPC as a marker of vascular health and prognosis of cardiovascular disease is already consolidated. This review aims to examine and evaluate recent data regarding EPC, as biomarkers, prognostic factor and potential therapy in cardiovascular disease.

scholarly journals Endothelial progenitor cells in age-related vascular remodeling

2018 ◽  
Vol 27 (5) ◽  
pp. 786-795 ◽  
Author(s):  
Jin-Xiu Yang ◽  
Yan-Yun Pan ◽  
Xing-Xiang Wang ◽  
Yuan-Gang Qiu ◽  
Wei Mao
Keyword(s):  
Endothelial Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Vascular Remodeling ◽  
Therapeutic Effects ◽  
Endothelial Progenitor ◽  
Age Related

Accumulating evidence has demonstrated that endothelial progenitor cells (EPCs) could facilitate the reendothelialization of injured arteries by replacing the dysfunctional endothelial cells, thereby suppressing the formation of neointima. Meanwhile, other findings suggest that EPCs may be involved in the pathogenesis of age-related vascular remodeling. This review is presented to summarize the characteristics of EPCs and age-related vascular remodeling. In addition, the role of EPCs in age-related vascular remodeling and possible solutions for improving the therapeutic effects of EPCs in the treatment of age-related diseases are discussed.

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