Differential gene expression during capillary morphogenesis in a microcarrier-based three-dimensional<i>in vitro</i>model of angiogenesis with focus on chemokines and chemokine receptors

Sun, Xueying; Zhang, Minyue; Shu, Chang; Li, Qiang; Yan, Xiao-Gui; Ni, Cheng; Qiu, Yudong; Ding, Yitao

doi:10.3748/wjg.v11.i15.2283

Cited by 20 publications

(13 citation statements)

References 35 publications

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“…A RayBio Human cytokine/growth factor antibody array identified several elevated factors in the supernatant, including inflammatory mediators with demonstrated roles in migration of mononuclear cells: IL-1h, Il-6, IL-8, IL-10, GRO, MCP-1, MIP1h, and RANTES [28,29]. Inflammation precedes angiogenesis, and several of the elevated cytokines from the CD133 À fraction (IL-8, GRO, MCP-1 and RANTES) have been implicated in regulating angiogenesis [30,31]. Studies have previously demonstrated interaction of progenitor cells and other sub-populations from the peripheral blood through cytokines, including the secretion of IL-8 and MCP-1 from CD14 + cells [15,32].…”

Section: Discussionmentioning

confidence: 99%

Generation of CD133+ cells from CD133− peripheral blood mononuclear cells and their properties

Suuronen

Wong

Kapila

et al. 2006

Cardiovascular Research

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These results demonstrate a source of blood CD133+ cells other than direct mobilization from the bone marrow. Cellular interaction was observed between fractions, with CD133+ cells showing better in vitro function in the presence of CD133- cells. These findings provide a novel source for CD133+ cells and a rationale for the investigation of angiogenic cell recruitment or delivery strategies involving more than one cell type at ischemic sites.

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Section: Discussionmentioning

confidence: 99%

Generation of CD133+ cells from CD133− peripheral blood mononuclear cells and their properties

Suuronen

Wong

Kapila

et al. 2006

Cardiovascular Research

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“…extent of vascularization was dependent on survivin expression, since survivin-deficient mice had a significant reduction in blood vessel density. Recent microarray studies have identified numerous novel genes associated with the proliferative, adhesive and remodelling phases of angiogenesis ( [78,79]; for reviews, see [80,81]). …”

Section: Figure 4 Potential Pathways Of Angiogenesis and Ec Apoptosismentioning

confidence: 99%

Can angiogenesis be exploited to improve stroke outcome? Mechanisms and therapeutic potential

et al. 2006

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Recent developments in our understanding of the pathophysiological events that follow acute ischaemic stroke suggest an important role for angiogenesis which, through new blood vessel formation, results in improved collateral circulation and may impact on the medium-to-long term recovery of patients. Future treatment regimens may focus on optimization of this process in the ischaemic boundary zones or 'penumbra' region adjacent to the infarct, where partially affected neurons exposed to intermediate perfusion levels have the capability of survival if perfusion is maintained or normalized. In this review, we present evidence that angiogenesis is a key feature of ischaemic stroke recovery and neuronal post-stroke re-organization, examine the signalling mechanisms through which it occurs, and describe the therapeutic potential of treatments aimed at stimulating revascularization and neuroprotection after stroke.

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“…Thus far a number of studies have been conducted that address the question, which genes are involved in capillary formation. Previous studies on gene profiling of angiogenic endothelium have focused on the isolation of endothelium from purely angiogenic and purely non-angiogenic conditions, such as EC embedded in collagen [6][7][8] or fibrin [9,10] matrices, or EC grown on matrigel [11]; EC isolated from tumor versus normal tissue [12,13]; or EC that had been stimulated with angiogenic factors with non-stimulated EC [14]. However, a comparison of gene expressions by tubule-forming and nontubule-forming endothelial cells that were both exposed to the same stimuli is still lacking.…”

Section: Introductionmentioning

confidence: 99%

Differential gene expression analysis of tubule forming and non-tubule forming endothelial cells: CDC42GAP as a counter-regulator in tubule formation

et al. 2007

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The formation of new tubular structures from a quiescent endothelial lining is one of the hallmarks of sprouting angiogenesis. This process can be mimicked in vitro by inducing capillary-like tubular structures in a three-dimensional (3D) fibrin matrix. We aimed to analyze the differential mRNA expression in two phenotypically distinct cell populations from the same culture, namely in tubule-forming endothelial cells and monolayer endothelial cells not participating in tubule formation. A fibrin-rich 3D matrix derived from human plasma was used to facilitate tubule formation by human foreskin microvascular endothelial cells (hMVEC). After 7 days of stimulation with VEGF, bFGF, and TNF-alpha, the culture consisted of a monolayer and capillary-like sprouts that had grown into the fibrinous matrix. A method was developed to separate the monolayer and tubule-forming populations of hMVEC, keeping their cellular integrity intact to ensure mRNA extraction and cDNA production. Subsequent array analysis resulted in an inventory of differentially expressed genes that were associated with either tube-forming (angiogenic) or non-angiogenic capacity. Differential gene expression was verified by real-time PCR on the original RNA samples as well as on RNA obtained from laser-capture microdissected cross sections of monolayers and capillary structures in the 3D fibrinous matrix. The expression of CDC42GAP, an inhibitor of active-state small Rho GTPases, was reduced in tubular hMVEC. Overexpression of CDC42GAP in hMVEC attenuated endothelial tubule formation, while its suppression by siRNA slightly enhanced this process. Thus, CDC42GAP was identified as a counter-regulatory mediator for tubule formation.

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Differential gene expression during capillary morphogenesis in a microcarrier-based three-dimensionalin vitromodel of angiogenesis with focus on chemokines and chemokine receptors

Abstract: The present study demonstrates a global profile of gene expression during endothelial capillary morphogenesis, and the results provide us much information about the molecular mechanisms of angiogenesis, with which further evaluation of individual genes can be conducted.

Cited by 20 publications

References 35 publications

Generation of CD133+ cells from CD133− peripheral blood mononuclear cells and their properties

Generation of CD133+ cells from CD133− peripheral blood mononuclear cells and their properties

Can angiogenesis be exploited to improve stroke outcome? Mechanisms and therapeutic potential

Differential gene expression analysis of tubule forming and non-tubule forming endothelial cells: CDC42GAP as a counter-regulator in tubule formation

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