Abstract
Abstract: :
Purpose:Small heat shock protein 27 (Hsp27) has previously been shown to have anti–apoptotic effects. Hsp 27 prevents the activation of procapase 9 by cytochrome c, which has been released from the mitochondria. Our goal was to measure the levels of Hsp27 and procaspase 9 subsequent to the onset of experimental glaucoma in Brown Norway rats. Methods:The IOP of the OS eye of Brown Norway (n=20) rats was elevated by injecting 1.9M NaCl solution into the episcleral veins using the Morrison model. The OD eye was used as a control. IOP was measured in awake animals with a Tonopen (Mentor, Norwell MA) before surgery and every other day after the saline injection. Following ten days of elevated IOP the retinas were removed and protein was isolated. Protein levels of Hsp 27 and procaspase 9 were determined by Western blot analysis and quantified by densitometry using beta–actin as a loading control. Statistics were analyzed using NCSS software to run a two way analysis of variance with the level of significance set at p<0.05. Results:The mean peak IOP for control eyes was 19.9 +/– 1.02, while the peak IOP for experimental eyes was 44.17 +/– 1.49. The mean IOP history, defined as the area under the pressure time curve, was 231.56 +/– 37.99. Hsp27 levels were increased significantly (p<0.05) in the glaucomatous eyes, while there was no change in the control eyes. Also, a significant increase of procaspase 9 (p<0.05) was observed in the glaucomatous eyes. There is a positive correlation between the increase of Hsp27 and procaspase 9 levels (R=.72). Conclusion:The increase in Hsp 27 protein levels is thought to prevent the cleavage of procaspase 9. It is assumed that preventing the activation of caspase 9, Hsp 27 inhibits the progression of the caspase cascade mediated by caspase 9.
Keywords: ganglion cells • apoptosis/cell death • intraocular pressure