Anti‐angiogenic property of edible berry in a model of hemangioma

Abstract

Hemangiomas represent a powerful model to study in vivo angiogenesis. Monocyte chemotactic protein 1 (MCP-1) is known to be responsible for recruiting macrophages to sites of infection or in£ammation and facilitate angiogenesis. Recently we have demonstrated that edible berry extracts potently suppress inducible vascular endothelial growth factor expression and in vitro angiogenesis. Comparative analysis of several berry extracts led to the observation that wild blueberry and a berry mix were most e¡ective. Our goal was to follow up on our ¢ndings with wild blueberry and the berry mix (OptiBerry). The present work rests on our current ¢nding that these two berry powders signi¢cantly inhibit inducible MCP-1 expression in endothelioma cells. Therefore, we sought to examine the effects of wild blueberry and berry mix in an in vivo model of experimental angiogenesis. Reporter studies showed that the berry powders signi¢cantly inhibited basal MCP-1 transcription and inducible nuclear factor U UB transcription. Endothelioma cells pre-treated with berry powders showed diminished ability to form hemangioma. Histological analysis demonstrated markedly decreased in¢ltration of macrophages in hemangioma of treated mice compared to placebo-treated controls. The current results provide the ¢rst in vivo evidence substantiating the antiangiogenic property of edible berries. ß

CCL2 Regulates Angiogenesis via Activation of Ets-1 Transcription Factor

“…Hemangiomas represent a powerful model to study in vivo angiogenesis for the several reasons: the angiogenic process is extremely potent; the rapid proliferation hemangioma is associated with macrophage infiltration, indicating an important role for the microenvironment in angiogenesis; and hemangiomas are commonly encountered in humans, providing important clinical relevance. Inoculation with polyoma middle T-transformed endothelial cells is also considered as a good autocrine model of angiogenesis and hemangioma (31,32). We felt that using bEnd.3 cells to evaluate CCL2-induced angiogenesis manner would have several advantages.…”

Anthocyanidins inhibit migration of glioblastoma cells: Structure‐activity relationship and involvement of the plasminolytic system

“…Consumption of anthocyanins has been shown to reduce the risk of coronary heart disease [Dell'Agli et al, 2004] and cancer [Hou, 2003]. Moreover, it has been reported that anthocyanins reduce the incidence of esophageal tumor [Kresty et al, 2001], reduce infiltration of macrophages in hemangioma [Atalay et al, 2003], and inhibit cell transformation [Xue et al, 2001], indicating potential cancer chemopreventive activity. While several studies indicate that anthocyanins exhibit strong scavenging of free radicals and antioxidant activities [Hou, 2003;Zheng and Wang, 2003], little is known about their antitumor activities.…”

Overexpression of Notch1 Ectodomain in Myeloid Cells Induces Vascular Malformations through a Paracrine Pathway

“…44 Interestingly, accumulation of myeloid cells (monocytes, macrophages, or dendritic cells) has been observed in infantile human hemangiomas 45,46 and in experimental hemangiomas. 47 In this latter model, inhibition of MCP-1 led to decreased infiltration of macrophages in hemangiomas and to diminished ability to form hemangiomas. 47 Our results confirm and extend these data by showing that N1 EC -expressing macrophages provide both pro-and anti-angiogenic signals.…”

“…47 In this latter model, inhibition of MCP-1 led to decreased infiltration of macrophages in hemangiomas and to diminished ability to form hemangiomas. 47 Our results confirm and extend these data by showing that N1 EC -expressing macrophages provide both pro-and anti-angiogenic signals.…”

“…29 Recently, an in vivo murine model of hemangioendothelioma was found to be totally dependent on MCP-1. 47,72 It is worth noticing that two (MCP-1 and FIII) of these genes represent known targets of the Egr-1 transcription factor, 30,59 whereas the other three (MCP-5, Jag1, and FXIII-A) harbor Egr-1 DNA-binding sequences (Figure 8). This strongly suggests that the Egr-1 represents a key intermediate in the N1 EC -mediated vascular disease of these Tg mice.…”