Fluctuations of the Intraocular Pressure in One Eye Influence the Intraocular Pressure in the Fellow Eye.

PURPOSE: To investigate the ophthalmotonic consensual reaction (OCR) in healthy individuals. METHODS: This was a cohort study of 59 pairs of eyes of patients who underwent cataract surgery in one eye and had no other ocular pathology than cataract. Main outcome measure was change of intraocular pressure (IOP) in the untreated fellow eye. The IOP was measured 1 hour before, 1 hour after, and 1 day after surgery. RESULTS: One hour after surgery, IOP decreased in 24 (41%) operated eyes (group A). In the corresponding untreated fellow eyes (group Af), the mean IOP (±standard deviation [SD]) did not change (14.1 ± 3.0 mmHg preoperatively to 14.2 ± 3.1 mmHg postoperatively, p = 0.8). Only two operated eyes showed unchanged IOP (group B). In 33 (56%) operated eyes, the IOP increased (group C). In the untreated fellow eyes (group Cf), the mean IOP decreased significantly from 15.1 ± 2.9 to 13.7 ± 2.6 mmHg (p = 0.0012). One day after surgery, the mean IOP of group Af decreased significantly from 14.2 ± 3.1 (postoperative IOP) to 12.7 ± 3.2 mmHg (p = 0.007). In group Cf, the mean IOP revealed no changes from 13.7 ± 2.6 to 13.5 ± 2.4 mmHg (p = 0.69). CONCLUSIONS: Our results showed some evidence for the existence of the OCR in healthy individuals. Significant IOP elevation in one eye resulted in IOP reduction in the fellow eye. Interestingly, this phenomenon did not exist vice versa.

Staurosporine-induced differentiation of the RGC-5 cell line leads to apoptosis and cell death at the lowest differentiating concentration.

BACKGROUND: Supplementation of staurosporine is the method of choice for differentiating the solely existing retinal ganglion cell (RGC)-5 cell line. This differentiation was initially claimed to be in the absence of apoptosis, but some publications supposed the induction of apoptosis during staurosporine induced RGC-5 differentiation. In respect to these inconsistencies in the literature, we investigated in detail whether RGC-5 cell differentiation by staurosporine induces apoptosis or not. METHODS: Amounts of 50 nM, 200 nM, 300 nM, and 600 nM of staurosporine were supplemented on RGC-5 cells for 24 h. Cell morphology and cell death, via propidium iodide staining, were evaluated with phase contrast and fluorescence microscopy, respectively. Cell amount, cell proliferation, and cell viability were analyzed by crystal violet staining, CFSE flow cytometry, and MTS assay, respectively. Apoptosis was determined by analyzing caspase 3/7 activity, Annexin-V+/ 7AAD- cells and the quotient of Bax to Bcl-2 mRNA expression via caspase 3/7 activity assay, flow cytometry, and real-time PCR, respectively. RESULTS: RGC-5 cells started to change their morphology and their expression of neuronal markers at 50 nM of staurosporine. This was associated with apoptosis and cell death, as indicated by a 2.1-fold (p < 0.0005) increase in caspase 3/7 activity, a 1.2-fold (p < 0.05) induction of Annexin-V+/ 7AAD- cells, and a 12-fold (p < 0.0005) increase in propidium iodide positive cells, respectively. Furthermore, staurosporine led to a dose-dependent increase in apoptosis and reduction in cell viability, cell density, and cell proliferation. CONCLUSIONS: The lowest staurosporine concentration inducing RGC-5 cell differentiation is accompanied by apoptosis and cell death.