The Complement Classical Pathway Is Activated In Murine Model Of Oxygen-induced Retinopathy

Purpose: To investigate whether the complement system is involved inmurine model of oxygen-induced retinopathy (OIR).Methods: Forty C57BL/6J newborn mice were divided randomly intoOIR group and normal group. For the normal group, the litters were raised inroom air. OIR was induced by exposing mice to75%±2%oxygen frompostnatal day7(P7) to P12and then recovered in room air. At the postnatalday17(P17), gene expressions of the complement components of theclassical pathway (CP), the mannose-binding lectin (MBL) pathway and thealternative pathway (AP) in the retina were determined by quantitativeRT-PCR. Basid on the PCR results, retinal protein expressions of the keycomponents of the complement system involved in the CP were examined byWestern blotting. Unpaired student’s t-test was used to assess thesignificance between the OIR and the normal groups. p<0.05was regardedas statistically significant.Results: Whole mounted retina in the OIR mice showed area of central hypoperfusion in both superficial and deep layers and neovascular tufts inthe periphery. The expressions of C1qb and C4b genes in the OIR retinawere significantly higher than those of the controls. The expression of retinalCFB gene in OIR mice was significantly lower than those of the normals.Howerer, the expressions of C3and CFH genes were higher. The proteinsynthesis of the key components of the complement system involved in theCP (C1q, C4and C3) were also significantly higher in OIR mouse retina.Althrough MASP1and MASP2were detected in both the OIR and thenormal groups, the expressions were weak and the difference between thetwo groups was not significant.Conclusions: Our data suggest that the complement system CP isactivated during the pathogenesis of murine model of oxygen-inducedretinopathy.