VEGF increases engraftment of bone marrow-derived endothelial progenitor cells (EPCs) into vasculature of newborn murine recipients

Young, Pampee P.; Hofling, A. Alex; Sands, Mark S.

doi:10.1073/pnas.182215799

Cited by 109 publications

(86 citation statements)

References 28 publications

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“…Recently, several investigators have established the presence of bone marrow-derived endothelial progenitor cells in the adult circulation and demonstrated that these cells contribute to glomerular healing, including glomerular capillary repair in experimental and human renal diseases (27)(28)(29). VEGF augments circulating endothelial progenitor cells and also induces engraftment of these cells into vasculature (30,31). In the present study, systemic administration of VEGF 165 can stimulate angiogenic capillary repair in damaged glomeruli and improves renal function in necrotizing and crescentic GN.…”

Section: Discussionsupporting

confidence: 58%

Vascular Endothelial Growth Factor165 Resolves Glomerular Inflammation and Accelerates Glomerular Capillary Repair in Rat Anti–Glomerular Basement Membrane Glomerulonephritis

Shimizu

Masuda²,

Mori³

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Vascular endothelial growth factor (VEGF) is essential for maintenance of the glomerular capillary network. The present study investigated the effects of VEGF in rats with progressive crescentic glomerulonephritis (GN). Necrotizing and crescentic GN was induced in rats by injection of anti-rat glomerular basement membrane (GBM) antibody. The alterations of glomerular capillaries and glomerular VEGF expression were assessed. In addition, the effects of continuous VEGF 165 administration (10 g/100 g per d) on glomerular capillaries, glomerular inflammation, and the course of crescentic GN were examined. The appropriate timing of VEGF administration in progressive GN also was evaluated. In anti-GBM GN, necrotizing and crescentic glomerular lesions occurred by day 7, and newly formed necrotizing lesions reoccurred by week 3. Expression of VEGF was markedly reduced in necrotizing and crescentic lesions. Capillary repair was impaired after capillary destruction in necrotizing and crescentic glomeruli, which rapidly progressed to sclerotic glomeruli with chronic renal failure. In contrast, in the rats that received VEGF 165 administration from day 7, the necrotizing and crescentic lesions recovered and renal function significantly improved in week 4. This was evident by proliferating endothelial cells and glomerular capillary repair. In addition, VEGF administration decreased intercellular adhesion molecule-1 and monocyte chemoattractant protein-1 expression in glomeruli (particularly on endothelial cells), reduced glomerular infiltrating CD8-postive and ED-1-positive cells, and inhibited the newly formed necrotizing lesions. VEGF administration was apparently effective against both the inflammatory and necrotizing glomerular lesions. These results suggest that VEGF administration resolves glomerular inflammation and accelerates glomerular recovery in the progressive necrotizing and crescentic GN. The therapeutic application of VEGF may be clinically useful for severe GN accompanied by extensive glomerular inflammation and endothelial injury.

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Section: Discussionsupporting

confidence: 58%

Vascular Endothelial Growth Factor165 Resolves Glomerular Inflammation and Accelerates Glomerular Capillary Repair in Rat Anti–Glomerular Basement Membrane Glomerulonephritis

Shimizu

Masuda²,

Mori³

et al. 2004

Journal of the American Society of Nephrology

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“…A causal relationship could be proved in the present model through inhibition of intraislet angiogenesis by using a selective inhibitor such as angiostatin. Further studies could examine an optimization of the AT dose, timing, or route of EPC delivery and/or coadministration of growth factors (15,48). To determine whether EPC are contributing to the increase in EC and affecting the increase in ␤-cell mass, it would be important to investigate changes in the number and mobilization of EPC after AT treatment.…”

Section: Discussionmentioning

confidence: 99%

Effects of atorvastatin on the regeneration of pancreatic β-cells after streptozotocin treatment in the neonatal rodent

Marchand

Arany

Hill

2010

American Journal of Physiology-Endocrinology and Metabolism

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Marchand KC, Arany EJ, Hill DJ. Effects of atorvastatin on the regeneration of pancreatic ␤-cells after streptozotocin treatment in the neonatal rodent. Am J Physiol Endocrinol Metab 299: E92-E100, 2010. First published April 13, 2010; doi:10.1152/ajpendo.00132.2010.-To investigate the role of statins in ␤-cell regeneration a model of streptozotocin (STZ)-induced ␤-cell injury was used in the neonatal rat. We hypothesized that ␤-cell growth and regeneration would increase following treatment with atorvastatin and that this would be associated with intraislet vasculogenesis. Pregnant Wistar rats were gavaged with 20 or 40 mg/kg atorvastatin for 21 days commencing on gestation day 15. Atorvastatin was detected in the circulation of the offspring. On postnatal day 4, the pups were given either a control or STZ (70 mg/kg ip) injection. ␤-Cell mass had partially recovered by postnatal day 44 following STZ treatment, and atorvastatin (20 mg/ kg) significantly increased ␤-cell mass in both STZ-treated and control animals. An increase in the numbers of small islets at postnatal day 44 was seen in STZ-treated animals following atorvastatin, suggestive of neogenesis, and glucose tolerance was improved. Treatment with atorvastatin caused an increase in the numbers of intraislet endothelial cells at postnatal day 14 and the percentage of endothelial cells undergoing DNA synthesis, suggesting that angiogenesis had preceded the increase in ␤-cell mass. The results indicate that functional ␤-cell mass was expanded with atorvastatin in both control and STZ-treated neonatal rats and suggests a novel effect of a statin in promoting islet plasticity.

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“…In vivo, both VEGF and GM-CSF increase the total numbers of bone marrow-derived endothelial cells, but whether this is simply because there are more blood vessels or instead due to an increase in the rate (i.e., percentage) of marrow-derived cell integration has not been examined in the adult. However, in the early postnatal period, VEGF stimulates a 10-fold increase in bone marrow-derived liver sinusoidal endothelial cells, with no concomitant increase in total sinusoidal endothelium, suggesting a VEGF-stimulated increase in the rate of progenitor cell integration (Young et al, 2002). Interestingly, in the heart, the increase in bone marrow-derived endothelial cells precisely parallels increases in vascularity, demonstrating tissue-to-tissue variability in progenitor function.…”

Section: Molecular Regulation Of Endothelial Cell Progenitorsmentioning

confidence: 95%

Hemangioblasts, angioblasts, and adult endothelial cell progenitors

Schatteman

Awad

2003

Anat. Rec.

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After decades of speculation, proof of embryonic hemangioblasts finally emerged a few years ago. Surprisingly, at about the same time, evidence for adult hemangioblasts began to appear, and recent single-cell bone marrow transplants have confirmed their existence. Embryonic and adult hemangioblasts appear to share antigenic determinants, including CD34, ACC133, and VEGFR2, although their phenotype may be plastic. They also respond to similar factors, prominent among them vascular endothelial growth factor (VEGF). In the adult, hemangioblasts reside principally in the bone marrow, although they may subsequently leave that niche to reside in nonhematopoietic tissues. A number of studies indicate that these cells or their progeny may be a significant source of endothelial cells in adult pathologic and nonpathologic vascularization, and may participate in vascular repair. In addition to hemangioblasts, a more differentiated source of endothelial cell progenitors may be present in the blood, namely, monocytes or monocytic-like cells. The relative importance of the two cell types in vivo is not clear, though endothelial cells derived from the two sources may not be identical, and hemangioblasts seem to provide a stimulus for differentiation of the monocytes. Treatment with exogenous bone marrow-derived cells can promote neovascularization, accelerate restoration of blood flow to ischemic tissues, and improve cardiac function after infarct. Hence, there is great hope that either alone, in combination with angiogenic factors, or as gene therapy vectors, we can harness these cells to treat ischemic and vascular diseases in the relatively near future. Anat Rec Part A 276A: 13-21, 2004.

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VEGF increases engraftment of bone marrow-derived endothelial progenitor cells (EPCs) into vasculature of newborn murine recipients

Cited by 109 publications

References 28 publications

Vascular Endothelial Growth Factor165 Resolves Glomerular Inflammation and Accelerates Glomerular Capillary Repair in Rat Anti–Glomerular Basement Membrane Glomerulonephritis

Vascular Endothelial Growth Factor165 Resolves Glomerular Inflammation and Accelerates Glomerular Capillary Repair in Rat Anti–Glomerular Basement Membrane Glomerulonephritis

Effects of atorvastatin on the regeneration of pancreatic β-cells after streptozotocin treatment in the neonatal rodent

Hemangioblasts, angioblasts, and adult endothelial cell progenitors

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