PURPOSE: To determine in rats whether there are time-dependent changes in interleukin-1 alpha (IL-1 alpha) and interleukin-1 beta (IL-1 beta) gene expression in transient retinal ischemia and to localize their mRNAs in the retina. METHODS: Retinal ischemia was induced in Sprague-Dawley rats by ligating the optic nerve. Two hours later, the ligature was released and reperfusion occurred. The levels of IL-1 alpha and IL-1 beta gene expression in the sensory retina were then compared at various times after reperfusion by a semiquantitative polymerase chain reaction method. Localization of their expressed mRNAs was examined by in situ hybridization histochemistry. RESULTS: Little expression of IL-1 alpha and IL-1 beta genes was observed in normal retina. IL-1 alpha gene expression rapidly increased (about 30-fold greater than that of the control) as early as 1 hour after cessation of ischemia, reached a peak (about 50-fold) at 3 to 12 hours, and then gradually decreased to near baseline levels. IL-1 beta gene expression began to increase 2 hours later than did that of IL-1 alpha and had two peaks. IL-1 beta gene was found by in situ hybridization histochemistry to be expressed by retinal glial cells, endothelial cells, and neutrophils infiltrating the retina and vitreous. No gene expression was found in the control retinas. CONCLUSIONS: Expression of IL-1 alpha and IL-1 beta genes was dramatically upregulated during reperfusion after induced retinal ischemia. IL-1 beta gene was expressed by retinal glial cells, endothelial cells, and neutrophils recruited into the retina. From these results, it appeared that IL-1 may have an important role in retinal ischemia-reperfusion injury.
PURPOSE: To determine in rats whether there are time-dependent changes in interleukin-1 alpha (IL-1 alpha) and interleukin-1 beta (IL-1 beta) gene expression in transient retinal ischemia and to localize their mRNAs in the retina. METHODS:Retinal ischemia was induced in Sprague-Dawley rats by ligating the optic nerve. Two hours later, the ligature was released and reperfusion occurred. The levels of IL-1 alpha and IL-1 beta gene expression in the sensory retina were then compared at various times after reperfusion by a semiquantitative polymerase chain reaction method. Localization of their expressed mRNAs was examined by in situ hybridization histochemistry. RESULTS: Little expression of IL-1 alpha and IL-1 beta genes was observed in normal retina. IL-1 alpha gene expression rapidly increased (about 30-fold greater than that of the control) as early as 1 hour after cessation of ischemia, reached a peak (about 50-fold) at 3 to 12 hours, and then gradually decreased to near baseline levels. IL-1 beta gene expression began to increase 2 hours later than did that of IL-1 alpha and had two peaks. IL-1 beta gene was found by in situ hybridization histochemistry to be expressed by retinal glial cells, endothelial cells, and neutrophils infiltrating the retina and vitreous. No gene expression was found in the control retinas. CONCLUSIONS: Expression of IL-1 alpha and IL-1 beta genes was dramatically upregulated during reperfusion after induced retinal ischemia. IL-1 beta gene was expressed by retinal glial cells, endothelial cells, and neutrophils recruited into the retina. From these results, it appeared that IL-1 may have an important role in retinal ischemia-reperfusion injury.