Effect Of MMPs And TIMPs On Traumatic PVR

PURPOSES: To investigate the expression of MMP-1, MMP-3 and TIMP-1 during thecourse of traumatic PVR treated with GM6001 and without GM6001, to explore thepotential role and mechanism of MMP-1, MMP-3 and TIMP-1 during the course oftraumatic PVR and to evaluate the effect of GM6001 on traumatic PVR prevention andtreatment.METHODS: 180 SD rats were divided randomly into three groups: normal controlgroup, the traumatic PVR group, the traumatic PVR treated with GM6001 group. Thenormal control group was intravitreous injected with normal saline. The traumatic PVRgroup was intravitreous injected with the riched platelet plasma. The traumatic PVRtreated with GM6001 group was intravitreous injected with the riched platelet plasmaand GM6001. The expression of MMP-1, MMP-3 and TIMP-1 were qualitative andsemiquantitative analysised with immunohistochemistry on day 1, 3, 7, 14, 21 and 28.RESULTS:1. Immunohistochemistry showed that the expression of MMP-1, MMP-3 and TIMP-1were mainly located in the photoreceptor cells layer, out plexiform layer, innerplexiform layer and nerve fiber layer.2. The expression of MMP-3 in the normal group and the traumatic PVR treated withGM6001 group were weak at all time. The expression of MMP-3 in the traumaticPVR group was strong at day 1, 3 and 7. The differences were statistical significance ascompared with the normal group and the traumatic PVR treated with GM6001 group(P＜0.01). The expression of MMP-3 in the traumatic PVR group decreased at thefollowing time.3. The expression of MMP-1 in the normal group and the traumatic PVR treated with GM6001 group were weak at all time. The expression of MMP-1 in the traumaticPVR group increased at day 3, reached the peak at day 7. The differences werestatistical significance as compared with the normal group and the traumatic PVRtreated with GM6001 group (P＜0.05). The expression of MMP-1 in the traumatic PVRgroup decreased at the following time.4. The expression of TIMP-1 in the traumatic PVR group and the traumatic PVRtreated with GM6001 group were strong at all time. The differences were statisticalsignificance as compared with the normal group (P＜0.01).5. The rate of MMP-3/TIMP-1 in the traumatic PVR group increased at day 1, 3 and7. The differences were statistical significance as compared with the normal group andthe traumatic PVR treated with GM6001 group (P＜0.05). The rate of MMP-1/TIMP-1in the traumatic PVR group increased at day 3, 7 and 14. The differences werestatistical significance as compared with the normal group and the traumatic PVRtreated with GM6001 group (P＜0.05).CONCLUSION: MMP-1 and MMP-3 played a key role in the course of traumaticPVR. TIMP-1 bound specifitly to MMP-1 and MMP-3 and suppressed their activity.GM6001 played an important role in the course of traumatic PVR prevention andtreatment by regulating the rate of MMP-1/TIMP-1 and MMP-3/TIMP-1.