Circadian intraocular pressure rhythm is generated by clock genes.

PURPOSE: The present study in a mouse model was undertaken to reveal the role of the circadian clock genes Cry1 and Cry2 in generation of 24-hour intraocular pressure (IOP) rhythm. METHODS: IOP was measured at eight time points daily (circadian time [CT] 0, 3, 6, 9, 12, 15, 18, and 21 hours), using a microneedle method in four groups of C57BL/6J mice (groups 1 and 3, wild-type; groups 2 and 4, Cry-deficient [Cry1-/-Cry2-/-]). During the IOP measurements, mice in groups 1 and 2 were maintained in a 12-hour light-dark cycle (LD), whereas mice in groups 3 and 4 were kept in a constant darkness (DD) that started 24 to 48 hours before the measurements. Circadian IOP variations in each group were evaluated by one-way analysis of variance (ANOVA) and Scheffé tests. RESULTS: In wild-type mice living in LD conditions, pressures measured in the light phase were significantly lower than those in the dark phase. This daily rhythm was maintained under DD conditions with low pressure in the subjective day and high pressure in the subjective night. In contrast, Cry-deficient mice did not show significant circadian changes in IOP, regardless of environmental light conditions. CONCLUSIONS: These findings demonstrate that clock oscillatory mechanisms requiring the activity of core clock genes are essential for the generation of a circadian rhythm of intraocular pressure.

Upregulation of transglutaminase in the goldfish retina during optic nerve regeneration.

To elucidate the molecular involvement of transglutaminase (TG) in central nervous system (CNS) regeneration, we cloned a full-length cDNA for neural TG (TG(N)) from axotomized goldfish retinas and produced a recombinant TG(N) protein from this cDNA. The levels of TG(N) mRNA and protein were increased at 10-30 days after optic nerve transection, and this increase in TG(N) was only localized in the ganglion cells in goldfish retinas. In retinal explant cultures, the recombinant TG(N) protein induced a drastic enhancement of neurite outgrowth, while TG(N)-specific RNAi significantly suppressed this neurite outgrowth. Taken together, these data strongly indicate that TG(N) is a key regulatory molecule for CNS regeneration.

In vivo confocal microscopy in the acute phase of corneal inflammation.

Two cases of noninfectious keratitis were studied using in vivo corneal confocal microscopy in addition to routine slit-lamp biomicroscopy. A 10-year-old boy suffered from keratitis in his left eye due to a bee sting and a 20-year-old man had keratitis following corneal blunt trauma. In both cases, we found a honeycomb pattern at the anterior and mid-stromal level of the middle cornea. This honeycomb pattern disappeared in 1 week with steroid treatment. This pattern might be caused by syncytial cell bodies of activated keratocytes, by focal corneal stroma edema, or by polymorphonuclear leukocyte infiltration along with the keratocytes or along preformed channels within the corneal stroma known as Bowman channels. Further analysis in a large number of patients may aid in further understanding in vivo human corneal inflammation.