December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Role of Smooth Muscle Cells and Pericytes in the Pathogenesis of Retinopathy of Prematurity (ROP)
Author Affiliations & Notes
  • T Chan-Ling
    Department of Anatomy University of Sydney Sydney Australia
  • L Baxter
    Department of Anatomy University of Sydney Sydney Australia
  • M Page
    Department of Anatomy University of Sydney Sydney Australia
  • S Hughes
    Department of Anatomy University of Sydney Sydney Australia
  • Footnotes
    Commercial Relationships   T. Chan-Ling, None; L. Baxter, None; M. Page, None; S. Hughes, None. Grant Identification: National Health and Medical Research Council of Australia, Baxter Perpetual Trust
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 1930. doi:
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      T Chan-Ling, L Baxter, M Page, S Hughes; Role of Smooth Muscle Cells and Pericytes in the Pathogenesis of Retinopathy of Prematurity (ROP) . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1930.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: The first stage of the kitten model of ROP is suppression of new vessel formation and vaso-obliteration of existing retinal vessels in the neonate, induced by hyperoxia-induced down regulation of VEGF expression by neuroglia. The second stage is characterised by hypoxia and pathological neovascularisation. Our aims were to determine whether the presence of desmin+ pericytes or alpha smooth muscle actin (SMA+) smooth muscle cells (smcs) prevents hyperoxia-induced vessel regression and whether mural cell abnormalities play a role in the pathogenesis of ROP. Methods: Kittens were exposed to 60-70% oxygen for 4 days and then returned to normoxia for 0, 3, 7, 10, 14, 17 and 27 days. Retinal wholemounts were double-labelled with antibodies against desmin, SMA and GS lectin. Results: During normal development, desmin+ pericytes were found from birth throughout the vascular plexus including newly formed vessels, whereas differentiating SMA+ smcs were present on the radial vessels. Hyperoxia resulted in the loss of vessels with desmin+ pericytes or SMA+ smcs. During the hypoxic stage of ROP, endothelial cells of the neovasculature adopted an abnormal rounded morphology. Desmin+ pericytes were present throughout the neovascular plexus and SMA+ smcs were associated with the radial vessels mimicking normal development. Intravitreal vascular membranes ensheathed with desmin+ mural cells were evident 10, 14, 17 and 27 days after return to room air. The intraretinal neovasculature and the pre-retinal vascular membranes were characterised by a reduced mural:endothelial cell ratio which subsequently recovered with the regression of pathology. Conclusion: During normal development and at various stages of ROP, pericyte ensheathment of vessels does not prevent normal and pathological angiogenesis. Further, immature pericytes and immature smcs do not prevent hyperoxia-induced vessel regression during retinal development in the cat. During hypoxic neovasculrisation, endothelial cell proliferation appears to outpace immature pericyte coverage. The reduced pericyte:endothelial cell ratio and the rounding up of vascular endothelial cells during the hypoxic phase of neovascularisation resemble the vascular changes observed with decreased expression of Ang-1 and/or increased expression of Ang-2.

Keywords: 572 retinopathy of prematurity • 614 vascular cells • 428 hypoxia 

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