Purpose

To evaluate the in vivo changes in the Schlemm's canal (SC) in patients with primary angle-closure glaucoma (PACG) after trabeculectomy using spectral-domain optical coherence tomography (SD-OCT).

Methods

Forty eyes of 40 patients with PACG who underwent trabeculectomy were included. All participants underwent SD-OCT. The diameter and area of SC were examined and measured before and within 1 month after trabeculectomy. All SD-OCT images were processed using adaptive compensation algorithm to improve contrast and image quality. Multivariate linear regression analysis was performed for predictors of percentage change in the mean SC diameter and area.

Results

The mean age of participants was 60.5 ± 14.6 years. Adaptive compensation significantly increased the percentage of sections in which SC was observable in the subjects studied from 52.5% (21/40) to 75.0% (30/40), which has acceptable intraobserver and interobserver repeatability. There was a significant increase in the SC diameter and area at the follow-up examination compared with the baseline value (SC diameter: 34.2 ± 6.2 μm vs. 28.4 ± 6.1 μm; SC area: 8117 ± 1942 μm(2) vs. 5200 ± 996 μm(2); all P < 0.001). After multivariate analysis, the only variable related to changes in SC was percentage change in IOP (SC diameter, P = 0.002; SC area, P < 0.001). In addition, the magnitude of the change in the SC area also correlated with angle opening distance at 750 μm from the scleral spur at baseline.

Conclusions

Expansion of SC was observed after trabeculectomy in PACG patients. The degree of SC expansion was related to the extent of the IOP decrease.

Reactive astrocytes influence post-injury recovery, repair, and pathogenesis of the mammalian CNS. Much of the regulation of astrocyte reactivity, however, remains to be understood. Using genetic loss and gain-of-function analyses in vivo, we show that the conserved MAP3K13 (also known as leucine zipper-bearing kinase [LZK]) promotes astrocyte reactivity and glial scar formation after CNS injury. Inducible LZK gene deletion in astrocytes of adult mice reduced astrogliosis and impaired glial scar formation, resulting in increased lesion size after spinal cord injury. Conversely, LZK overexpression in astrocytes enhanced astrogliosis and reduced lesion size. Remarkably, in the absence of injury, LZK overexpression alone induced widespread astrogliosis in the CNS and upregulated astrogliosis activators pSTAT3 and SOX9. The identification of LZK as a critical cell-intrinsic regulator of astrocyte reactivity expands our understanding of the multicellular response to CNS injury and disease, with broad translational implications for neural repair.