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01) (Fig.?3). M��ller cell migration was significantly inhibited by TGF-�� (10?ng/ml) to almost half the migration of controls (p? to M��ller cells. Endothelial cells in TGF-�� showed a similar migration pattern to controls (p? on M��ller cell proliferation except at higher concentrations (20?ng/ml). These findings suggest that the combined effects of TGF-�� and FGF-2 could contribute to the differential growth responses of endothelial cells and M��ller cells observed during normal retinal development and in pathology. Demarcation of the incipient fovea is a perplexing issue. At no time during development is the incipient or developing fovea vascularized (Provis & Hendrickson 2008). As vessels approach the incipient fovea, their rate of growth decreases, and endothelial cell proliferation is decreased in the vicinity of the incipient fovea and along the horizontal meridian, compared to the rest of the retina (Sandercoe et?al. 2003). It has been suggested that antiproliferative and/or antiangiogenic factor(s) are differentially expressed along the horizontal meridian and concentrated at the incipient fovea. As well as controlling proliferation, these factors could limit migration of key cell types to produce a complex morphological pattern consistent with that observed during foveal development. Consequently, the presence of such factor(s) would play an important role in preventing vessel growth into the central fovea (Provis 2001). The expression of such factor/s would need to occur prior to any physical marking of the FAZ by the vasculature and associated cell types. Indeed, it has been reported recently that the antiangiogenic factors, PEDF and brain natriuretic peptide, along with the guidance factor EphA6, are highly expressed in the developing foveal region (Kozulin et?al. 2009a,b). Several growth factors including VEGF, TGF-�� and FGF-2 are involved in the highly complex and well-controlled processes of primate retinal vascular development (Sandercoe et?al.2003; Cornish et?al. 2005).