Limits...
Changes in expression of aquaporin-4 and aquaporin-9 in optic nerve after crushing in rats.

Suzuki H, Oku H, Horie T, Morishita S, Tonari M, Oku K, Okubo A, Kida T, Mimura M, Fukumoto M, Kojima S, Takai S, Ikeda T - PLoS ONE (2014)

Bottom Line: The results showed that the expression of AQP4 was increased on day 1 but the level was significantly lower than that in the sham group on days 4 and 7 (P<0.05).The expression of AQP4 and GFAP was reduced at the crushed site where AQP4-negative and AQP9-positive astrocytes were present.The presence of AQP9-positive astrocytes at the crushed site may counteract the metabolic damage but this change did not fully compensate for the barrier function defect.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Osaka Medical College, Osaka, Japan.

ABSTRACT
The purpose of this study was to determine the temporal and spatial changes in the expression of AQP4 and AQP9 in the optic nerve after it is crushed. The left optic nerves of rats were either crushed (crushed group) or sham operated (sham group), and they were excised before, and at 1, 2, 4, 7, and 14 days later. Four optic nerves were pooled for each time point in both groups. The expression of AQP4 and AQP9 was determined by western blot analyses. Immunohistochemistry was used to determine the spatial expression of AQP4, AQP9, and GFAP in the optic nerve. Optic nerve edema was determined by measuring the water content in the optic nerve. The barrier function of the optic nerve vessels was determined by the extravasated Evans blue dye on days 7 and 14. The results showed that the expression of AQP4 was increased on day 1 but the level was significantly lower than that in the sham group on days 4 and 7 (P<0.05). In contrast, the expression of AQP9 gradually increased, and the level was significantly higher than that in the sham group on days 7 and 14 (P<0.05, Tukey-Kramer). The down-regulation of AQP4 was associated with crush-induced optic nerve edema, and the water content of the nerve was significantly increased by 4.3% in the crushed optic nerve from that of the untouched fellow nerve on day 7. The expression of AQP4 and GFAP was reduced at the crushed site where AQP4-negative and AQP9-positive astrocytes were present. The barrier function was impaired at the crushed site on days 7 and 14, restrictedly where AQP4-negative and AQP9-positive astrocytes were present. The presence of AQP9-positive astrocytes at the crushed site may counteract the metabolic damage but this change did not fully compensate for the barrier function defect.

No MeSH data available.


Related in: MedlinePlus

Double labeling of AQP9 and CD68 at the crushed site on day 7.Representative photographs from 3 independent samples are presented with higher magnifications in the right column. Arrows indicate crush sites. CD68 positive cells are present between the AQP9 positive fibrils suggesting that microglia/macrophages are not the cellular sources for AQP9 after crushing the optic nerve.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4257723&req=5

pone-0114694-g007: Double labeling of AQP9 and CD68 at the crushed site on day 7.Representative photographs from 3 independent samples are presented with higher magnifications in the right column. Arrows indicate crush sites. CD68 positive cells are present between the AQP9 positive fibrils suggesting that microglia/macrophages are not the cellular sources for AQP9 after crushing the optic nerve.

Mentions: The expression of AQP9 was enhanced at the crushed site (Figure 6), and the immunoreactivity to AQP9 had a honeycomb appearance. The site was also immunopositive to GFAP (Figure 6A) and nestin (Figure 6B), another intermediate filament protein of astrocytes. There was an accumulation of microglia/macrophages at the crushed site on day 7 as reported earlier (Figure 7). However, immunoreactivity to AQP9 was not co-localized with that of CD68 (Figure 7). Thus, AQP9 was over-expressed in the astrocytes at the crushed site where the expression of AQP4 was down-regulated.


Changes in expression of aquaporin-4 and aquaporin-9 in optic nerve after crushing in rats.

Suzuki H, Oku H, Horie T, Morishita S, Tonari M, Oku K, Okubo A, Kida T, Mimura M, Fukumoto M, Kojima S, Takai S, Ikeda T - PLoS ONE (2014)

Double labeling of AQP9 and CD68 at the crushed site on day 7.Representative photographs from 3 independent samples are presented with higher magnifications in the right column. Arrows indicate crush sites. CD68 positive cells are present between the AQP9 positive fibrils suggesting that microglia/macrophages are not the cellular sources for AQP9 after crushing the optic nerve.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4257723&req=5

pone-0114694-g007: Double labeling of AQP9 and CD68 at the crushed site on day 7.Representative photographs from 3 independent samples are presented with higher magnifications in the right column. Arrows indicate crush sites. CD68 positive cells are present between the AQP9 positive fibrils suggesting that microglia/macrophages are not the cellular sources for AQP9 after crushing the optic nerve.
Mentions: The expression of AQP9 was enhanced at the crushed site (Figure 6), and the immunoreactivity to AQP9 had a honeycomb appearance. The site was also immunopositive to GFAP (Figure 6A) and nestin (Figure 6B), another intermediate filament protein of astrocytes. There was an accumulation of microglia/macrophages at the crushed site on day 7 as reported earlier (Figure 7). However, immunoreactivity to AQP9 was not co-localized with that of CD68 (Figure 7). Thus, AQP9 was over-expressed in the astrocytes at the crushed site where the expression of AQP4 was down-regulated.

Bottom Line: The results showed that the expression of AQP4 was increased on day 1 but the level was significantly lower than that in the sham group on days 4 and 7 (P<0.05).The expression of AQP4 and GFAP was reduced at the crushed site where AQP4-negative and AQP9-positive astrocytes were present.The presence of AQP9-positive astrocytes at the crushed site may counteract the metabolic damage but this change did not fully compensate for the barrier function defect.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Osaka Medical College, Osaka, Japan.

ABSTRACT
The purpose of this study was to determine the temporal and spatial changes in the expression of AQP4 and AQP9 in the optic nerve after it is crushed. The left optic nerves of rats were either crushed (crushed group) or sham operated (sham group), and they were excised before, and at 1, 2, 4, 7, and 14 days later. Four optic nerves were pooled for each time point in both groups. The expression of AQP4 and AQP9 was determined by western blot analyses. Immunohistochemistry was used to determine the spatial expression of AQP4, AQP9, and GFAP in the optic nerve. Optic nerve edema was determined by measuring the water content in the optic nerve. The barrier function of the optic nerve vessels was determined by the extravasated Evans blue dye on days 7 and 14. The results showed that the expression of AQP4 was increased on day 1 but the level was significantly lower than that in the sham group on days 4 and 7 (P<0.05). In contrast, the expression of AQP9 gradually increased, and the level was significantly higher than that in the sham group on days 7 and 14 (P<0.05, Tukey-Kramer). The down-regulation of AQP4 was associated with crush-induced optic nerve edema, and the water content of the nerve was significantly increased by 4.3% in the crushed optic nerve from that of the untouched fellow nerve on day 7. The expression of AQP4 and GFAP was reduced at the crushed site where AQP4-negative and AQP9-positive astrocytes were present. The barrier function was impaired at the crushed site on days 7 and 14, restrictedly where AQP4-negative and AQP9-positive astrocytes were present. The presence of AQP9-positive astrocytes at the crushed site may counteract the metabolic damage but this change did not fully compensate for the barrier function defect.

No MeSH data available.


Related in: MedlinePlus