Angiotensin II promotes NO production, inhibits apoptosis and enhances adhesion potential of bone marrow-derived endothelial progenitor cells

Yin, Tao; Ma, Xin‐Liang; Zhao, Li; Cheng, Kun; Wang, Haichang

doi:10.1038/cr.2008.69

Cited by 51 publications

(39 citation statements)

References 33 publications

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“…Rat bone marrow-derived MNCs were isolated by density gradient centrifugation with Ficoll, as previously described (Yin et al 2008). MNCs were seeded on fibronectin-coated plates at a density of 10 6 cells per cm 2 in EGM-2MV (Lonza, Verviers/B, Endothelial cell basal medium-2, plus FBS, VEGF, R 3 -IGF-1, rhEGF, rhFGF-B, GA-1000, hydrocortisone and ascorbic acid).…”

Section: Animalsmentioning

confidence: 99%

“…Cell proliferation EPC proliferative capacity was measured using the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay as previously described (Yin et al 2008). After serum starvation for 24 h, cells were treated with PIN (1.25-200 mg/L, Sigma) dissolved in DMSO or pretreated with PI3-kinase inhibitor (LY294002) or NOS inhibitor (L-NAME) before treatment with PIN.…”

Section: Measuring the Biological Functions Of Epcsmentioning

confidence: 99%

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Pinocembrin, a major flavonoid in propolis, improves the biological functions of EPCs derived from rat bone marrow through the PI3K-eNOS-NO signaling pathway

et al. 2012

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The number and quality of endothelial progenitor cells (EPCs) are damaged to varying degrees in patients at risk for developing atherosclerosis. The improvement of the quantity and functions of EPCs can enhance repair of injured endothelial monolayer resulting in inhibiting atherosclerosis. The purpose of this study was to investigate the effect of pinocembrin (PIN), a major flavonoid in propolis on the differentiation and biological functions of EPCs and the potential mechanisms of these effects. Flow cytometry analysis revealed that PIN treatment increased the number of CD34? , CD133 ?

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Section: Animalsmentioning

confidence: 99%

Section: Measuring the Biological Functions Of Epcsmentioning

confidence: 99%

Pinocembrin, a major flavonoid in propolis, improves the biological functions of EPCs derived from rat bone marrow through the PI3K-eNOS-NO signaling pathway

et al. 2012

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“…In vitro studies have shown that eNOS/NO signaling enhance the mobilization, homing, and adhesion of EPCs (35,36). eNOS/NO signaling is associated with BPD (13).…”

Section: Lung Enos and Vegf Were Increased When Combining Epcs Transpmentioning

confidence: 99%

Combined iNO and endothelial progenitor cells improve lung alveolar and vascular structure in neonatal rats exposed to prolonged hyperoxia

Sun

Qian

2015

Pediatr Res

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Background: Stem cells or inhaled nitric oxide (iNO) are reported to improve lung structures in bronchopulmonary dysplasia (BPD) models. We hypothesized that combined iNO and transplanted endothelial progenitor cells (EPCs) might restore lung structure in rats after neonatal hyperoxia. Methods: Litters were separated into eight groups: room air, hyperoxia, hyperoxia + iNO, hyperoxia + iNO + L-NAME, hyperoxia + EPCs, hyperoxia + EPCs + L-NAME, hyperoxia + EPCs + iNO, and hyperoxia + EPCs + iNO + L-NAME. Litters were exposed to hyperoxia from the 21st day, then, sacrificed. EPCs were injected on the 21st day. L-NAME was injected daily for 7 d from the 21st day. Serum vascular endothelial growth factor (VEGF), radial alveolar count (RAC), VIII factor, EPCs engraftment, lung VEGF, VEGFR2, endothelial nitric oxide (eNOS) and SDF-1 expression, and NO production were examined. results: Hyperoxia exposure led to air space enlargement, loss of lung capillaries, and low expression of VEGF and eNOS. Transplanted EPCs, when combined with iNO, had significantly increased engraftment in lungs, compared to EPCs alone, upon hyperoxia exposure. There was improvement in alveolarization, microvessel density, and upregulation of VEGF and eNOS proteins in the hyperoxia-exposed EPCs with iNO group, compared to hyperoxia alone. conclusion: Combined EPCs and iNO improved lung structures after neonatal hyperoxia. This was associated with the upregulation of VEGF and eNOS expression.B ronchopulmonary dysplasia (BPD) is a chronic lung disease associated with significant mortality and morbidity in premature infants. New BPD is characterized by arrested alveolar and vascular growth (vascular hypothesis of BPD) (1,2). Alveolar formation is a highly coordinated process between the development of airways and pulmonary vasculature (3). Exposure to inflammation caused by excessive O 2 supplementation is hypothesized to interfere with the coordinated process of normal human lung development. Neonatal hyperoxia exposure is known to disrupt alveolar formation and growth, providing a useful model for studying BPD (4).Cell-based therapy is a novel approach that offers much promise in the prevention and treatment of BPD, including embryonic stem cells, mesenchymal stem cells, placental stem cells, umbilical cord stem cells, amniotic fluid and amnionderived cells, and lung progenitor cells. Endothelial progenitor cells (EPCs) are precursors of endothelial cells, which have the capacity of self-renewal and proliferation. EPCs is one of the key cells mediating vascular growth, which can mobilize from bone marrow and home to the site of vascular injuries, promoting neovascularization (5). There is data showing that reduced numbers or dysfunction of EPCs at birth is associated with the development of BPD (6,7). In addition, a reduction in the number of EPCs in the bone marrow, circulation and lungs has also emerged in animal models of BPD (8). Evidences that angiogenic cells treatment can restore lung structure have been demonstrated. Balasubramaniam et al...

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“…The more acute stimulatory effects in cultured EPCs depend on AT 1 R-mediated facilitation of vascular endothelial growth factor-mediated NO release, involving an increased vascular endothelial growth factor receptor and endothelial NO synthase expression, as well as antiapoptotic phosphatidylinositol 3/Akt signaling. 2,7 The chronic, deleterious effects on cultured EPCs depend on ROS release, and accumulation of damage to macromolecules, in particular to DNA, might be a necessary, timeconsuming interlude between ROS release and induction of …”

mentioning

confidence: 99%

“…This is in sharp contrast with the antiapoptotic, proangiogenic effect of Ang II on EPCs that was observed in other studies. 2,7,8 These stimulatory effects of Ang II takes place on a shorter term (Յ5 days). Therefore, the paradoxical findings seem to be based on a temporal difference in exposure to Ang II.…”

mentioning

confidence: 99%

Angiotensin II Deteriorates Endothelial Progenitor Cells

Roks

2011

Hypertension

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A pproximately 15 years ago it was discovered that the bone marrow and blood harbor stem cells with angiogenic potential. 1 Because some of these stem cells express endothelial markers, it is believed that they are endothelial progenitor cells (EPCs) that will contribute to the maintenance of the circulatory system and develop into adult endothelial cells. Many studies followed to unravel the physiological role and the therapeutic application of EPCs. All of these research endeavors did not yet lead to a consensus regarding the identification of true EPCs, and EPC quantification remains subjective. 2 To complicate matters even more, it has now been proposed that nonendothelial CD31 ϩ bone marrow cells participate in neovascularization. 3 It is, therefore, not only complicated for the investigator to compose a satisfactory study design but also for the reader to evaluate the results. Preferably, such studies investigate circulating, as well as cultured EPCs, and provide proof of their involvement in (patho)physiology through functional studies. Identification of circulating EPCs should be identified by combining stem cell markers with endothelial cell markers, whereas EPCs obtained from cultured blood, bone marrow, or spleen-derived mononuclear cells (MNCs) should be identified on the basis of endothelial markers and variables of angiogenic function. 2 It is according to these favorable requirements that, in this issue of Hypertension, Endtmann et al 4 show that treatment of adherent, cultured human blood MNCs with angiotensin (Ang) II decreases early outgrowth EPC numbers, colony formation, and migration via Ang II type 1 receptor (AT 1 R) stimulation and that a 12-day infusion of Ang II reduces the numbers of circulating EPCs in wild-type mice. Novel evidence for the involvement of AT 1 Rs in the regulation of vascular repair function of progenitor cells was obtained by studying the effect of wild-type versus AT 1 R Ϫ/Ϫ spleenderived MNCs on neointima formation and re-endothelialization after carotid artery injury in mice. Through an elegant series of experiments, Endtmann et al 4 show that AT 1 R signaling inhibits the endothelial repair function of MNCs. In addition, bone marrow replacement studies in apolipoprotein E Ϫ/Ϫ mice suggest that bone marrow AT 1 Rs play a role in atherogenesis. The in vivo studies do not illuminate whether the AT 1 R-mediated effects are conferred by EPCs, by other MNCs, or bone marrow cell types. However, because the angiogenic potential of progenitor cells does not entirely depend on true EPCs, 3 this question seems more academic than of clinical interest. The in vitro results (see Figure 1 of the article by Endtmann et al 4 ) show that non-EPC MNC types are also affected and emphasize the importance of studying the immunomodulatory role of Ang II in vascular disease, a field of research that is gaining attention. In all likelihood, an interplay between EPCs and inflammatory cells exists that is of utmost importance for the vasoprotective effects of pharmacological renin-angioten...

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Angiotensin II promotes NO production, inhibits apoptosis and enhances adhesion potential of bone marrow-derived endothelial progenitor cells

Cited by 51 publications

References 33 publications

Pinocembrin, a major flavonoid in propolis, improves the biological functions of EPCs derived from rat bone marrow through the PI3K-eNOS-NO signaling pathway

Pinocembrin, a major flavonoid in propolis, improves the biological functions of EPCs derived from rat bone marrow through the PI3K-eNOS-NO signaling pathway

Combined iNO and endothelial progenitor cells improve lung alveolar and vascular structure in neonatal rats exposed to prolonged hyperoxia

Angiotensin II Deteriorates Endothelial Progenitor Cells

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