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Greene, Arin K.; Wiener, Stephen M.; Puder, Mark; Yoshida, Akitoshi; Shi, Bin; Perez‐Atayde, Antonio R.; Efstathiou, Jason A.; Holmgren, Lars; Adamis, Anthony P.; Rupnick, Maria A.; Folkman, Judah; O’Reilly, Michael

doi:10.1097/00000658-200304000-00015

Cited by 22 publications

(16 citation statements)

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“…Our hypothesis that neovascularization contributes to AVM progression was supported by the finding that Stage III lesions had greater microvasculature compared to Stage II AVMs. Any enlarging lesion requires neovascularization to support its increasing tissue mass through the process of angiogenesis (growth of new blood vessels from pre-existing vasculature), 9–14 or vasculogenesis ( de novo formation of new vasculature). 17–21 Because all AVMs had a greater endothelial proliferative index than control tissue, angiogenesis may be contributing to its growth.…”

Section: Discussionmentioning

confidence: 99%

“…Although AVM has been considered a quiescent lesion, as evidenced by endothelial turnover, 8 the endothelium of different staged lesions has not been studied. Because increasing tissue mass requires neovascularization, 9–14 we hypothesized that expansion of AVM may be dependent on angiogenesis and/or vasculogenesis. The purpose of this study was to determine if more severe AVMs exhibit increased angiogenic/vasculogenic factors compared to lower-staged lesions.…”

Section: Introductionmentioning

confidence: 99%

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Increased Endothelial Progenitor Cells and Vasculogenic Factors in Higher-Staged Arteriovenous Malformations

Bischoff

Mulliken

et al. 2011

Plastic and Reconstructive Surgery

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Introduction Arteriovenous malformations (AVMs) cause significant morbidity, primarily because they expand over time and recur after treatment. We hypothesized that neovascularization might contribute to AVM progression. Methods AVM tissue was prospectively collected from 12 patients after resection. Schobinger stage was determined by clinical history. Neovascularization in Stage II lesions (n=7) was compared to Stage III AVMs (n=5) that had progressed. Specimens were analyzed using immunohistochemistry for CD31, Ki67, and CD34/CD133. Quantitative real-time RT-PCR (qRT-PCR) was used to determine mRNA expression of factors that recruit endothelial progenitor cells (EPCs): vascular endothelial growth factor (VEGF), stromal derived factor-1α (SDF-1α), and hypoxia-inducible factor-1 α (HIF-1α). VEGF receptors (VEGFR1, VEGFR2, neuropilin 1, 2) also were quantified using qRT-PCR. Results Stage III AVMs showed greater microvessel density (5.8%) than Stage II lesions (1.3%) (p=0.004); no difference in proliferating endothelial cells was noted (p=0.67). CD133+CD34+ EPCs were elevated in Stage III (0.53%) compared to Stage II AVMs (0.25%) (p=0.03). HIF-1α and SDF-1α were increased 7.6 and 7.9 fold in Stage III, compared to Stage II lesions (1.7 fold and 3.3 fold), respectively (p=0.02). Neuropilin 1 and neuropilin 2 expression was greater in Stage III (5.8 fold and 4.6 fold) than Stage II AVMs (3.0 fold and 2.4 fold) (p=0.03). Conclusion Higher-staged AVMs exhibit increased expression of EPCs and factors that stimulate their recruitment. Neovascularization by vasculogenesis may be involved in progression of AVM.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Increased Endothelial Progenitor Cells and Vasculogenic Factors in Higher-Staged Arteriovenous Malformations

Bischoff

Mulliken

et al. 2011

Plastic and Reconstructive Surgery

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“…The modulation of endothelial cell proliferation or apoptosis has been shown to affect liver regeneration after partial hepatectomy in mice [23]. During liver regeneration the expression and activity of proapoptotic pathways is inhibited and after massive liver resection the activation of apoptosis is a major cause for failure of regeneration [24].…”

Section: Discussionmentioning

confidence: 99%

The combined effect of erythropoietin and granulocyte macrophage colony stimulating factor on liver regeneration after major hepatectomy in rats

et al. 2010

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BackgroundThe liver presents a remarkable capacity for regeneration after hepatectomy but the exact mechanisms and mediators involved are not yet fully clarified. Erythropoietin (EPO) and Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) have been shown to promote liver regeneration after major hepatectomy.Aim of this experimental study is to compare the impact of exogenous administration of EPO, GM-CSF, as well as their combination on the promotion of liver regeneration after major hepatectomy.MethodsWistar rats were submitted to 70% major hepatectomy. The animals were assigned to 4 experimental groups: a control group (n = 21) that received normal saline, an EPO group (n = 21), that received EPO 500 IU/kg, a GM-CSF group (n = 21) that received 20 mcg/kg of GM-CSF and a EPO+GMCSF group (n = 21) which received a combination of the above. Seven animals of each group were killed on the 1st, 3rd and 7th postoperative day and their remnant liver was removed to evaluate liver regeneration by immunochemistry for PCNA and Ki 67.ResultsOur data suggest that EPO and GM-CSF increases liver regeneration following major hepatectomy when administered perioperatively. EPO has a more significant effect than GM-CSF (p < 0.01). When administering both, the effect of EPO seems to fade as EPO and GM-CSF treated rats have decreased regeneration compared to EPO administration alone (p < 0.01).ConclusionEPO, GM-CSF and their combination enhance liver regeneration after hepatectomy in rats when administered perioperatively. However their combination has a weaker effect on liver regeneration compared to EPO alone. Further investigation is needed to assess the exact mechanisms that mediate this finding.

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“…Resection of two thirds of the total liver mass results in stimulation of quiescent hepatocytes, and activation of numerous transcription factors that modulate many genes involved in the proliferation of hepatocytes [38–40]. An exponential increase in the number of hepatocytes leads to definitive architectural and functional changes in the liver; avascular clusters of cells are generated that induce the differentiation and subsequent replication of the other types of hepatic cells, notably liver sinusoidal endothelial cells (LSECs), hepatic stellate cells (HSCs), and other EC precursors mobilized from the bone marrow.…”

Section: Physiological Angiogenesismentioning

confidence: 99%

Angiogenesis: From Chronic Liver Inflammation to Hepatocellular Carcinoma

Sanz-Cameno

Trapero-Marugán

Chaparro

et al. 2010

Journal of Oncology

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Recently, new information relating to the potential relevance of chronic hepatic inflammation to the development and progression of hepatocellular carcinoma (HCC) has been generated. Persistent hepatocellular injury alters the homeostatic balance within the liver; deregulation of the expression of factors involved in wound healing may lead to the evolution of dysplastic lesions into transformed nodules. Progression of such nodules depends directly on the development and organization of a vascular network, which provides the nutritional and oxygen requirements to an expanding nodular mass. Angiogenic stimulation promotes intense structural and functional changes in liver architecture and physiology, in particular, it facilitates transformation of dysplasia to nodular lesions with carcinogenic potential. HCC depends on the growth and spreading of vessels throughout the tumor. Because these vascular phenomena correlate with disease progression and prognosis, therapeutic strategies are being developed that focus on precluding vascular expansion in these tumors. Accordingly, an in-depth study of factors that promote and support pathological angiogenesis in chronic hepatic diseases may provide insights into methods of preventing the development of HCC and/or stimulating the regression of established HCC.

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Cited by 22 publications

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Increased Endothelial Progenitor Cells and Vasculogenic Factors in Higher-Staged Arteriovenous Malformations

Increased Endothelial Progenitor Cells and Vasculogenic Factors in Higher-Staged Arteriovenous Malformations

The combined effect of erythropoietin and granulocyte macrophage colony stimulating factor on liver regeneration after major hepatectomy in rats

Angiogenesis: From Chronic Liver Inflammation to Hepatocellular Carcinoma

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