Differential effects of vascular growth factors on arterial and venous angiogenesis

Abstract

The angiogenic stimulators VEGF and naltrexone induce development of veins and arteries in a proportional manner. In contrast, the angiogenic inhibitors OGF and retinoic acid demonstrated a greater inhibitory effect on arterial as compared with venous angiogenesis. Such differential effects on angiogenesis may be important in both defining mechanisms of action and designing therapeutic interventions.

Antiangiogenic properties of carotenoids: A potential role of maize as functional food

“…Despite some controversial effects of retinoic acid (RA) as an VEGFinduced angiogenesis and tubulogenesis promoter (Tanabe et al, 2004;Saito et al, 2006), previous reports (Majewskia et al, 1995;Pal et al, 2000;Blebea et al, 2002) demonstrated the inhibitory action of RA on the VEGF-induced angiogenesis in the normal human skin and tumor cell lineages (Kim et al, 2006). Additionally to RA, astaxanthin and other carotenoids also selectively inhibited the angiogenic response induced by VEGF in the CAM assay of chick embryos, which is in accordance with our findings.…”

Embryonic Blastemic Changes in Retinoic Acid-Induced Hindlimb Deformity

“…It is known that RA concentration does affect vessel formation [Bouman et al, 1995;Wendling et al, 2000]; however, the effect of RA on endothelial cells is still controversial. Although it is considered an angiogenic inhibitor [Pal et al, 2000;Blebea et al, 2002], it has also been shown that RA can stimulate endothelial cell proliferation and differentiation in vitro [Burgess and Hall, 2001;Gaetano et al, 2001], and it can also induce angiogenesis in vivo [Gaetano et al, 2001]. These observations could help explain our results showing an increased volume of vascular lumen.…”

The OGF–OGFr Axis Utilizes the p16INK4aand p21WAF1/CIP1Pathways to Restrict Normal Cell Proliferation

“…The action of the OGF-OGFr axis in normal and cancer cells is targeted to DNA synthesis McLaughlin, 1987, 1991;Isayama et al, 1991;Zagon et al, 1994Zagon et al, , 1995bZagon et al, , 2000aMcLaughlin, 1996;McLaughlin and Wu, 1998;McLaughlin et al, 1999;Wilson et al, 2000;Blebea et al, 2002). In squamous cell carcinoma of the head and neck, OGF activity has been shown to be dependent on one CKI, p16…”

“…Because OGF depresses DNA synthesis and subsequent cell/tissue growth in a wide variety of normal and developing cells in humans and animals, including ectodermal, mesodermal, and endodermal derivatives Hauser and Stiene-Martin, 1991;Isayama et al, 1991;Zagon and McLaughlin, 1991;Zagon et al, 1994Zagon et al, , 1995bZagon et al, , 1996aZagon et al, ,b, 1997Zagon et al, , 1999bMcLaughlin, 1996;Vertes et al, 1996;McLaughlin and Wu, 1998;Blebea et al, 2000Blebea et al, , 2002Wilson et al, 2000;Kornyei et al, 2003), the question arises as to the mechanism of peptide action on the cell cycle in these cells. The present investigation examined the specific target(s) in the cell cycle for the OGF-OGFr axis in cells derived from four normal human tissues: umbilical vein endothelial This article was published online ahead of print in MBC in Press (http://www.molbiolcell.org/cgi/doi/10.1091/mbc.E08 -07-0681) on October 15, 2008. cells (HUVECs), epidermal keratinocytes (NHEKs), dermal fibroblasts (NHDFs), and mesenchymal stem cells (hMSCs).…”