scholarly journals Endothelial progenitor cells, endothelial cell dysfunction and much more: observations from cardiac syndrome X

Heart ◽  
2007 ◽  
Vol 93 (9) ◽  
pp. 1020-1021 ◽  
Author(s):  
P. K Y Goon ◽  
G. Y H Lip
Keyword(s):  
Endothelial Cell ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Syndrome X ◽  
Endothelial Cell Dysfunction ◽  
Cardiac Syndrome X ◽  
Endothelial Progenitor ◽  
Cell Dysfunction ◽  
Cardiac Syndrome

scholarly journals Circulating endothelial progenitor cells in patients with cardiac syndrome X

Heart ◽  
2007 ◽  
Vol 93 (9) ◽  
pp. 1071-1076 ◽  
Author(s):  
H. Shmilovich ◽  
V. Deutsch ◽  
A. Roth ◽  
H. Miller ◽  
G. Keren ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Syndrome X ◽  
Cardiac Syndrome X ◽  
Endothelial Progenitor ◽  
Circulating Endothelial Progenitor Cells ◽  
Cardiac Syndrome

scholarly journals Endothelial Progenitor Cells in Acute Ischemic Kidney Injury: Strategies for Increasing the Cells' Renoprotective Competence

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
D. Patschan ◽  
S. Patschan ◽  
G. A. Müller
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Kidney Injury ◽  
Peripheral Circulation ◽  
Microvascular Endothelial Cell ◽  
Protective Effects ◽  
Endothelial Cell Dysfunction ◽  
Endothelial Progenitor ◽  
Cell Dysfunction ◽  
Peritubular Capillaries

Acute ischemic kidney injury is the most frequent cause of acute renal failure in daily clinical practice. It has become increasingly recognized that microvascular endothelial cell dysfunction (ED) in peritubular capillaries inhibits the process of postischemic renal reperfusion. ED can serve as therapeutic target in the management of acute ischemic kidney injury. Postischemic reflow can be restored by systemic administration of either mature endothelial cells or of endothelial progenitor cells. Endothelial progenitor cells EPCs can be cultured from the peripheral circulation of humans and different animals. The cells act vasoprotectively by direct and indirect mechanisms. The protective effects of EPCs in acute ischemic kidney injury can be stimulated by preincubating the cells with different agonistic mediators. This paper summarizes the currently available data on strategies to improve the renoprotective activity of EPCs in acute ischemic kidney injury.

Abstract 894: Leptin Potentiates the Angiogenic Properties of Endothelial Progenitor Cells In Vitro and In Vivo

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Nana-Maria Heida ◽  
Marco R Schroeter ◽  
I-Fen Cheng ◽  
Elena I Deryugina ◽  
Thomas Korff ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Tube Length ◽  
Endothelial Progenitor ◽  
Signal Transduction Inhibitors ◽  
Stimulation Of

Endothelial progenitor cells (EPC) have been reported to contribute to neovascularization. We have previously shown that the adipocytokine leptin may enhance the adhesive properties of EPC by upregulating specific integrins. To investigate whether the angiogenic effects of leptin may be mediated by modulation of EPC function, mononuclear cells were isolated from healthy human volunteers and cultivated under endothelial cell conditions for 7 days. In the matrigel assay, pretreatment of EPC with recombinant leptin for 24 hours dose-dependently enhanced their incorporation into tubular structures provided by mature endothelial cells. For example, 138.3 ± 7.6% (P = 0.001) and 145.3 ± 5.5% (P = 0.0001) CM-DiI-labeled EPC were detected after stimulation with 10 and 100 ng/mL leptin, respectively (control-treated EPC defined as 100%). Furthermore, in the spheroid angiogenesis assay, stimulation of EPC with 10 ng/mL leptin increased the number of sprouts (P < 0.0001) and tube length (P < 0.0001) of coincubated mature endothelial cells, and the outgrowth of EPC (P < 0.0001). Addition of 100-fold excess of leptin-neutralizing or leptin-receptor-binding antibodies completely reversed these effects. Moreover, EPC adhesion onto endothelial cell tubules could be reduced by addition of RGD peptides (from 159 ± 13.7% to 101.8 ± 14.6%; P = 0.02), or of neutralizing antibodies against αvβ3 (from 165.3 ± 11.8% to 103.8 ± 13.3%; P = 0.006) or αvβ5 (to 93.5 ± 15.8%; P = 0.005). Further experiments using specific signal transduction inhibitors (10 μM of LY294002, PD98059, or SB203580), as well as Western blot analysis, revealed that leptin signaling in EPC involves phosphoinositide-3 kinase and p42/44, but not by p38 MAP kinase. The effects of leptin could also be confirmed under in vivo conditions. Stimulation of EPC with 100 ng/mL leptin potentiated the insprout of newly formed avian vessels into collagen onplants placed on the chorion allantoic membrane of chicken embryos (angiogenic index, 0.58 ± 0.24) compared to control-treated EPC (0.44 ± 0.27; P = 0.07) and endothelial basal medium alone (0.31 ± 0.26; P = 0.0007). Thus, our in vitro and in vivo results suggest that the angiogenic effects of leptin may partly depend on its specific interaction with endothelial progenitor cells.

scholarly journals Angiogenesis‐Related Genes in Endothelial Progenitor Cells May Be Involved in Sickle Cell Stroke

2020 ◽  
Vol 9 (3) ◽  
Author(s):  
Mirta T. Ito ◽  
Sueli M. da Silva Costa ◽  
Letícia C. Baptista ◽  
Gabriela Q. Carvalho‐Siqueira ◽  
Dulcinéia M. Albuquerque ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cell ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Sickle Cell ◽  
Cell Biology ◽  
Vascular Diseases ◽  
Clinical Aspects ◽  
Endothelial Progenitor ◽  
Matrix Metalloproteinase 1

Background The clinical aspects of sickle cell anemia ( SCA ) are heterogeneous, and different patients may present significantly different clinical evolutions. Almost all organs can be affected, particularly the central nervous system. Transient ischemic events, infarcts, and cerebral hemorrhage can be observed and affect ≈25% of the patients with SCA . Differences in the expression of molecules produced by endothelial cells may be associated with the clinical heterogeneity of patients affected by vascular diseases. In this study, we investigated the differential expression of genes involved in endothelial cell biology in SCA patients with and without stroke. Methods and Results Endothelial progenitor cells from 4 SCA patients with stroke and 6 SCA patients without stroke were evaluated through the polymerase chain reaction array technique. The analysis of gene expression profiling identified 29 differentially expressed genes. Eleven of these genes were upregulated, and most were associated with angiogenesis (55%), inflammatory response (18%), and coagulation (18%) pathways. Downregulated expression was observed in 18 genes, with the majority associated with angiogenesis (28%), apoptosis (28%), and cell adhesion (22%) pathways. Remarkable overexpression of the MMP 1 (matrix metalloproteinase 1) gene in the endothelial progenitor cells of all SCA patients with stroke (fold change: 204.64; P =0.0004) was observed. Conclusions Our results strongly suggest that angiogenesis is an important process in sickle cell stroke, and differences in the gene expression profile of endothelial cell biology, especially MMP 1 , may be related to stroke in SCA patients.

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