Technical notes on endothelial progenitor cells: Ways to escape from the knowledge plateau

Fadini, Gian Paolo; Baesso, Ilenia; Albiero, Mattia; Sartore, Saverio; Agostini, Carlo; Avogaro, Angelo

doi:10.1016/j.atherosclerosis.2007.12.039

Cited by 234 publications

(232 citation statements)

References 54 publications

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“…8,46,47 Therefore, clinical correlation data such as provided by our study are useful to attribute more biological relevance to one putative EPC phenotype vs. the others. For example, one could speculate that CD34+KDR+ cell phenotype may correlate with pathological vascular damage and increased CV risk, 48 while CD133+KDR+ and CD34+CD133+KDR+ are likely related to oxidative status and endothelial function as suggested by their status in BS/GS that is, increased CD133+KDR+ and CD34+CD133+KDR+ and unchanged CD34+KDR+, which fits with the biochemical, molecular and functional picture of good endothelial status reported in these patients. [16][17][18][19][20][21][22][23][26][27][28] In conclusion, the study documents in a human system that EPC numbers and specific populations are related to important clinical and biochemical factors involved in CV status.…”

Section: Discussionsupporting

confidence: 77%

Endothelial progenitor cells relationships with clinical and biochemical factors in a human model of blunted angiotensin II signaling

et al. 2011

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Angiotensin II (Ang II) is essential for endothelial progenitor cells (EPCs) function as Ang-II-induced oxidative stress causes senescence of EPCs and endothelial dysfunction and Ang II type 1 receptor blockers increase EPCs. Moreover, EPCs activity is dependent on nitric oxide (NO) and heme oxygenase (HO)-1 as these correlate with EPCs senescence and are reduced in hypertensives. Bartter's/Gitelman's syndrome patients (BS/GS), have increased Ang II yet normo/hypotension along with blunted Ang II signaling, reduced oxidative stress, increased NO and HO-1, thus presenting a unique system to explore EPC biology and its relationship with vascular clinical and biochemical correlates. Circulating EPCs, NO-dependent vasodilation (flow-mediated dilation (FMD)) and HO-1 gene expression were characterized in 10 BS/GS patients and in 10 normotensive subjects. EPCs defined by cell surface antigens CD34+kinase-insert domain receptor (KDR+), CD133+KDR+ and CD133+CD34+KDR+ cells were quantitiated via direct three-color flow-cytometry analysis, HO-1 gene expression by reverse transcription-PCR and FMD by B-mode echo scan of the right brachial artery. Correlation analysis was carried out regarding FMD and EPCs, FMD and HO-1 and EPCs and HO-1. In BS/GS, CD34+KDR+ cell numbers did not differ from controls while CD133+KDR+ and CD133+CD34+ KDR+ cell numbers were higher. HO-1 gene expression, as well as FMD, was higher in BS/GS compared with controls. Both CD133+KDR+ and CD133+CD34+KDR+ strongly correlated with both FMD and HO-1. FMD and HO-1 were also strongly correlated. These results document in a human system that EPC numbers and specific populations are related to important clinical and biochemical factors involved in cardiovascular (CV) status and reaffirm the utility of BS/GS patients as a useful system to investigate EPC's role(s) in the pathophysiology of cardiovascular remodeling in humans.

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Section: Discussionsupporting

confidence: 77%

Endothelial progenitor cells relationships with clinical and biochemical factors in a human model of blunted angiotensin II signaling

et al. 2011

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“…Interestingly, miR-146a expression was validated in CACs obtained from CHF patients and CTR subjects. This ex vivo cellular model was chosen because CACs are involved in vascular renewal and can be easily purified from peripheral blood, and CACs obtained from CHF patients have a distinguishing feature of senescence (Olivieri et al 2012;Fadini et al 2008;Rehman et al 2003). A 1,000-fold increase of miR-146a expression along with a strong reduction of IRAK1 expression was observed in CACs of CHF patients compared to CTR.…”

Section: Discussionmentioning

confidence: 99%

MiR-146a as marker of senescence-associated pro-inflammatory status in cells involved in vascular remodelling

Olivieri

Lazzarini

Recchioni

et al. 2012

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185

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In order to identify new markers of vascular cell senescence with potential in vivo implications, primary cultured endothelial cells, including human umbilical vein endothelial cells (HUVECs), human aortic endothelial cells (HAECs), human coronary artery endothelial cells (HCAECs) and ex vivo circulating angiogenic cells (CACs), were analysed for microRNA (miR) expression. Among the 367 profiled miRs in HUVECs, miR-146a, miR-9, miR-204 and miR-367 showed the highest up-regulation in senescent cells. Their predicted target genes belong to nine common pathways, including Toll-like receptor signalling (TLR) that plays a pivotal

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“…BOECs belong to the family of endothelial progenitor cells (EPCs), which harbors a heterogeneous selection of different cell types, participating in and modulating neovascularization. Distinct EPC subtypes are defined using different culture techniques and/or combinations of cell surface markers 1, 2, 3. BOECs, also referred to as circulating endothelial colony‐forming cells (ECFCs) or late outgrowth EPCs, are the only cell type featuring the characteristics of a “true” EPC, given that these cells are self‐renewing, clonogenic, and able to form capillary‐like structures and integrate into functional blood vessels in vitro and in vivo, respectively 4…”

Section: Introductionmentioning

confidence: 99%

Neovascularization Potential of Blood Outgrowth Endothelial Cells From Patients With Stable Ischemic Heart Failure Is Preserved

Dauwe

Pelacho

Wibowo

et al. 2016

JAHA

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BackgroundBlood outgrowth endothelial cells (BOECs) mediate therapeutic neovascularization in experimental models, but outgrowth characteristics and functionality of BOECs from patients with ischemic cardiomyopathy (ICMP) are unknown. We compared outgrowth efficiency and in vitro and in vivo functionality of BOECs derived from ICMP with BOECs from age‐matched (ACON) and healthy young (CON) controls.Methods and ResultsWe isolated 3.6±0.6 BOEC colonies/100×106 mononuclear cells (MNCs) from 60‐mL blood samples of ICMP patients (n=45; age: 66±1 years; LVEF: 31±2%) versus 3.5±0.9 colonies/100×106 MNCs in ACON (n=32; age: 60±1 years) and 2.6±0.4 colonies/100×106 MNCs in CON (n=55; age: 34±1 years), P=0.29. Endothelial lineage (VEGFR2+/CD31+/CD146+) and progenitor (CD34+/CD133−) marker expression was comparable in ICMP and CON. Growth kinetics were similar between groups (P=0.38) and not affected by left ventricular systolic dysfunction, maladaptive remodeling, or presence of cardiovascular risk factors in ICMP patients. In vitro neovascularization potential, assessed by network remodeling on Matrigel and three‐dimensional spheroid sprouting, did not differ in ICMP from (A)CON. Secretome analysis showed a marked proangiogenic profile, with highest release of angiopoietin‐2 (1.4±0.3×105 pg/106 ICMP‐BOECs) and placental growth factor (5.8±1.5×103 pg/106 ICMP BOECs), independent of age or ischemic disease. Senescence‐associated β‐galactosidase staining showed comparable senescence in BOECs from ICMP (5.8±2.1%; n=17), ACON (3.9±1.1%; n=7), and CON (9.0±2.8%; n=13), P=0.19. High‐resolution microcomputed tomography analysis in the ischemic hindlimb of nude mice confirmed increased arteriogenesis in the thigh region after intramuscular injections of BOECs from ICMP (P=0.025; n=8) and CON (P=0.048; n=5) over vehicle control (n=8), both to a similar extent (P=0.831).Conclusions BOECs can be successfully culture‐expanded from patients with ICMP. In contrast to impaired functionality of ICMP‐derived bone marrow MNCs, BOECs retain a robust proangiogenic profile, both in vitro and in vivo, with therapeutic potential for targeting ischemic disease.

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Technical notes on endothelial progenitor cells: Ways to escape from the knowledge plateau

Cited by 234 publications

References 54 publications

Endothelial progenitor cells relationships with clinical and biochemical factors in a human model of blunted angiotensin II signaling

Endothelial progenitor cells relationships with clinical and biochemical factors in a human model of blunted angiotensin II signaling

MiR-146a as marker of senescence-associated pro-inflammatory status in cells involved in vascular remodelling

Neovascularization Potential of Blood Outgrowth Endothelial Cells From Patients With Stable Ischemic Heart Failure Is Preserved

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