Endothelial cell markers from clinician's perspective

Rakočević, Jelena; Orlić, Dejan; Ajtić, Olivera Mitrović; Tomasević, M; Dobrić, Milan; Zlatić, Nataša; Milašinović, Dejan; Stanković, Goran; Ostojić, Miodrag; Labudović‐Borović, Milica

doi:10.1016/j.yexmp.2017.02.005

Cited by 73 publications

(57 citation statements)

References 140 publications

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“…Finally, CYP46A1 immunolocalization was conducted in retinal flat mounts and cross sections, which were also stained for CD31, a marker of vascular endothelial cells, or neuronal-specific nuclear protein, a DNA-binding protein that identifies many populations of mature neurons. 61,62 In both flat mounts and cross sections, the immunoreactivity for CYP46A1 overlapped in part with that for CD31 ( Figure 10A). There was also CYP46A1 immunoreactivity outside retinal blood vessels, which could reflect CYP46A1 expression in some of the retinal neurons.…”

Section: Gene Expression In Retinal Endothelial Cells and Rpementioning

confidence: 96%

Retinal Vascular Abnormalities and Microglia Activation in Mice with Deficiency in Cytochrome P450 46A1–Mediated Cholesterol Removal

Saadane

Mast

Trichonas

et al. 2019

The American Journal of Pathology

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Section: Gene Expression In Retinal Endothelial Cells and Rpementioning

confidence: 96%

Retinal Vascular Abnormalities and Microglia Activation in Mice with Deficiency in Cytochrome P450 46A1–Mediated Cholesterol Removal

Saadane

Mast

Trichonas

et al. 2019

The American Journal of Pathology

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“…These studies speculated the potential prognostic inferiority of pan-endothelial markers (i.e vWF, CD31, CD34) was caused by the additional staining of pre-existing angiogenically inactive vessels [23]. In contrast, many studies have shown that CD105 predominantly stain proliferating endothelial cells [22, 33, 38–46]. However, a few studies have observed CD105-positive vessels in normal [47] and GBM-adjacent brain tissue [48], and the marker needs further validation.…”

Section: Discussionmentioning

confidence: 99%

“…The MVDs were immunohistochemically assessed by means of two endothelial markers: von Willebrand factor (vWF or FVIII related antigen), a pan-endothelial marker [22], which illustrates the metabolic demand of the tumor [23]; and endoglin (CD105), a marker of proliferating endothelial cells [24], which reflects the degree of angiogenesis [23]. In addition, we investigated the correlation between the MVDs and their associations with the histopathological features thromboses, high cellular density, high vascular density, and mitotic count.…”

Section: Introductionmentioning

confidence: 99%

Angiogenesis and radiological tumor growth in patients with glioblastoma

et al. 2018

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BackgroundThe preoperative growth of human glioblastomas (GBMs) has been shown to vary among patients. In animal studies, angiogenesis has been linked to hypoxia and faster growth of GBM, however, its relation to the growth of human GBMs is sparsely studied. We have therefore aimed to look for associations between radiological speed of growth and microvessel density (MVD) counts of the endothelial markers vWF (Factor VIII related antigen) and CD105 (endoglin).MethodsPreoperative growth was estimated from segmented tumor volumes of two preoperative T1-weighted postcontrast magnetic resonance imaging scans taken ≥14 days apart in patients with newly diagnosed GBMs. A Gompertzian growth curve was computed from the volume data and separated the patients into two groups of either faster or slower tumor growth than expected. MVD counts of the immunohistochemical markers von Willebrand factor (vWF) (a pan-endothelial marker) and CD105 (a marker of proliferating endothelial cells) were assessed for associations with fast-growing tumors using Mann-Whitney U tests and a multivariable binary logistic regression analysis.ResultsWe found that only CD105-MVD was significantly associated with faster growth in a univariable analysis (p = 0.049). However, CD105-MVD was no longer significant when corrected for the presence of thromboses and high cellular density in a multivariable model, where the latter features were significant independent predictors of faster growth with respective odds ratios 4.2 (95% confidence interval, 1.2, 14.3), p = 0.021 and 2.6 (95% confidence interval, 1.0, 6.5), p = 0.048.ConclusionsMVDs of neither endothelial marker were independently associated with faster growth, suggesting angiogenesis-independent processes contribute to faster glioblastoma growth.Electronic supplementary materialThe online version of this article (10.1186/s12885-018-4768-9) contains supplementary material, which is available to authorized users.

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“…VEGF играет важнейшую роль в таких процессах, как деградация базальной мембраны ЭК и внеклеточного матрикса, пролиферация ЭК, формирование капилляров, синтез новой базальной мембраны. Таким образом, VEGF оказывается вовлечен во все этапы ангиогенеза [39,46]. Изоформа VEGF-A существует в виде 4 различных подтипов: VEGF121, VEGF165, VEGF189 и VEGF206 [51] и считается первым ростовым фактором, характерным именно для ЭК, который появляется в ходе эмбрионального развития.…”

Section: Introductionunclassified

“…Именно VEGF-A является ключевой молекулой, индуцирующей васкулогенез и ангиогенез [39]. VEGF-A был открыт как фактор проницаемости сосудов, затем была показана его роль в пролиферации, миграции, про растании сосудов и формировании трубок сосудов [13,39]. Сильнейшим стимулом, вызывающим секрецию VEGF, является гипоксия.…”

Section: Introductionunclassified

Influence of VEGF deprivation upon vascular formation by endothelium in the presence of macrophages

et al. 2020

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Development of angiogenesis depends on the functional state of endothelial cells, as well as on the balanced secretion of cytokines, growth factors and chemokines by endothelial cells and cells of microenvironment. Macrophages represent an essential component of the microenvironment and take part in the formation of blood vessels both due to the production of cytokines and due to contact interactions with endothelial cells. VEGF is among the most important cytokines that control angiogenesis at all its stages. Currently, the role of VEGF in the intercellular interactions of endothelial cells and macrophages is not well described. The aim of our study was to investigate the effect of VEGF deprivation using monoclonal antibodies on angiogenesis under conditions of co-cultivation of endothelium and macrophages. Materials and methods: monoclonal antibodies to VEGF-A were used for VEGF deprivation in monoculture of endothelial cells and in co-culture of endothelial cells with macrophages. The IL-1β, IL-6 and TNFα cytokines were used as inducers. When VEGF-A was removed from the medium, endothelial cells show plasticity and form longer vessels, they modify the expression of VEGF receptors. Macrophages regulate endothelial cell activity through the secretion of cytokines, including VEGF, and through contact interactions with endothelial cells. THP-1 cells increase the sensitivity of endothelial cells to VEGF by stimulating the VEGFR1 and VEGFR3 expression, this effect is VEGF-A-independent. The IL-1β, IL-6, TNFa cytokines independently stimulate non-branching angiogenesis, increasing the length of the vessels. At the same time, IL-ip increases the VEGFR1 expression on the surface of endothelial cells. In contrast, IL-6 and TNFα decrease it, thereby regulating the sensitivity of endothelial cells to VEGF. The effects of these cytokines are not dependent on VEGF-A. The IL-1β, IL-6, TNFα cytokines promote acquisition of anti-angiogenic properties by THP-1 cells that is independent on VEGF-A, as well as on expression of its receptors by endothelial cells. Thus, VEGF is an important, but not the sole factor controlling angiogenesis. Under conditions of VEGF-A deficiency, either endothelial cells or microenvironment cells are able to compensate for its functional load due to the production of other growth factors.

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Endothelial cell markers from clinician's perspective

Cited by 73 publications

References 140 publications

Retinal Vascular Abnormalities and Microglia Activation in Mice with Deficiency in Cytochrome P450 46A1–Mediated Cholesterol Removal

Retinal Vascular Abnormalities and Microglia Activation in Mice with Deficiency in Cytochrome P450 46A1–Mediated Cholesterol Removal

Angiogenesis and radiological tumor growth in patients with glioblastoma

Influence of VEGF deprivation upon vascular formation by endothelium in the presence of macrophages

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