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Z. Shao, A. L. Dorfman, P. Sapieha, P. Lachapelle, S. Chemtob; Choroidal Vasculature Degeneration in Oxygen Induced Retinopathy: The Role of 15deoxy-12, 14-Prostagladin J2 . Invest. Ophthalmol. Vis. Sci. 2010;51(13):4463.
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To investigate the contribution of choroidal vascular involution to the retinal functional changes associated with retinopathy of prematurity (ROP) and determine the involvement of 15deoxy-Δ12, 14-Prostagladin J2 (15d-PGJ2), a potent anti-inflammatory and important anti-angiogenic factor, in this process.
Two different rat models of oxygen induced retinopathy (OIR; 80% O2 or 50%/10% (24hr cycle) from postnatal day (P) 1-P14) were used to mimic ROP. Retinal function was assessed by multifocal electroretinogram (mfERG) at P60 and compared to controls raised in room air (21% O2). Structural changes were assessed in open sections and drifts in protein expression patterns were determined by immunohistochemistry on cryo-sagittal sections. Choroidal vascular density and morphology was determined by eye corrosion casts examined by scanning electron microscopy (SEM) while vessel leakage was assessed following intra-cardiac injections of Evans blue. Levels of 15d-PGJ2 were measured by ELISA immunoassay and 15d-PGJ2 was delivered intravitreally to room air animals to investigate the in vivo cytotoxic effect of this compound on choroidal vasculature.
Pronounced and predominantly central choroidal vascular involution (choroidal vascular thickness and choriocapillary vessel density) was detected in both models of OIR animals and was accompanied by increased choroidal vessel leakage. This translated to a significant loss of function largely restricted to the central retina (when compared to the periphery) as determined by mfERG. Relevantly, 15d-PGJ2 levels increased dramatically during the first week of hyperoxic exposure coinciding with the initial apoptotic nuclei in the choroid. Confirmation of the involvement of 15d-PGJ2 in choroidal involution was obtained after its intraocular administration to normal animals compromised choroidal vasculature in an analogous manner to OIR.
The involvement of choroidal decay in the progression of ROP has to date not been addressed. Our data demonstrates that central choroidal involution is associated with the cardinal retinal dysfunction associated with ROP and suggests that effective future therapeutic strategies should take this vascular bed into consideration.
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