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Trehalose treatment accelerates the healing of UVB-irradiated corneas. Comparative immunohistochemical studies on corneal cryostat sections and corneal impression cytology.
Histol Histopathol. 2012 08; 27(8):1029-40.HH

Abstract

The UVB-irradiated cornea is damaged by oxidative stress. Toxic oxygen products induced by UVB radiation in the cornea are insufficiently removed by antioxidants, whose numbers decrease with increasing UVB irradiation. In addition, the UVB-irradiated cornea suffers from hypoxic conditions because damaged corneal cells cannot utilize oxygen normally, although the supply of oxygen to the cornea is unchanged (normal). This contributes to attenuated re-epithelialization, corneal neovascularization and apoptotic cell death. Our previous publications reported that trehalose applied on the corneal surface during irradiation significantly suppressed UVB-induced corneal oxidative damage. The results of this study provide for the first time important evidence that trehalose applied on the surface of corneas for two weeks following repeated UVB irradiation (312 nm, daily dose 0.5 J/cm2) accelerated corneal healing, restored corneal transparency and suppressed corneal neovascularization. Compared to buffered saline treatment, following which caspase-3, nitrotyrosine, malondialdehyde and urokinase-type plasminogen activator were still strongly expressed in the corneal epithelium two weeks after irradiation and corneal neovascularization was evident, apoptotic cell death was already significantly reduced after one week of trehalose application. The expression of other markers of injury returned to normal levels during two weeks of trehalose treatment. In conclusion, our results show that trehalose accelerated healing of the UVB irradiated cornea, very probably via suppression of hypoxia-response injury. In addition, immunohistochemical results on corneal cryostat sections corresponded with those obtained using corneal impression cytologies, thus confirming that corneal impression cytologies are useful for diagnostic purposes.

Authors+Show Affiliations

Laboratory of Eye Histochemistry and Pharmacology, Institute of Experimental Medicine, Center of Excellence, Academy of Sciences of Czech Republic, Prague, Czech Republic. cejkova@biomed.cas.czNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22763875

Citation

Cejková, Jitka, et al. "Trehalose Treatment Accelerates the Healing of UVB-irradiated Corneas. Comparative Immunohistochemical Studies On Corneal Cryostat Sections and Corneal Impression Cytology." Histology and Histopathology, vol. 27, no. 8, 2012, pp. 1029-40.
Cejková J, Cejka C, Luyckx J. Trehalose treatment accelerates the healing of UVB-irradiated corneas. Comparative immunohistochemical studies on corneal cryostat sections and corneal impression cytology. Histol Histopathol. 2012;27(8):1029-40.
Cejková, J., Cejka, C., & Luyckx, J. (2012). Trehalose treatment accelerates the healing of UVB-irradiated corneas. Comparative immunohistochemical studies on corneal cryostat sections and corneal impression cytology. Histology and Histopathology, 27(8), 1029-40. https://doi.org/10.14670/HH-27.1029
Cejková J, Cejka C, Luyckx J. Trehalose Treatment Accelerates the Healing of UVB-irradiated Corneas. Comparative Immunohistochemical Studies On Corneal Cryostat Sections and Corneal Impression Cytology. Histol Histopathol. 2012;27(8):1029-40. PubMed PMID: 22763875.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Trehalose treatment accelerates the healing of UVB-irradiated corneas. Comparative immunohistochemical studies on corneal cryostat sections and corneal impression cytology. AU - Cejková,Jitka, AU - Cejka,Cestmír, AU - Luyckx,Jacques, PY - 2012/7/6/entrez PY - 2012/7/6/pubmed PY - 2012/11/7/medline SP - 1029 EP - 40 JF - Histology and histopathology JO - Histol Histopathol VL - 27 IS - 8 N2 - The UVB-irradiated cornea is damaged by oxidative stress. Toxic oxygen products induced by UVB radiation in the cornea are insufficiently removed by antioxidants, whose numbers decrease with increasing UVB irradiation. In addition, the UVB-irradiated cornea suffers from hypoxic conditions because damaged corneal cells cannot utilize oxygen normally, although the supply of oxygen to the cornea is unchanged (normal). This contributes to attenuated re-epithelialization, corneal neovascularization and apoptotic cell death. Our previous publications reported that trehalose applied on the corneal surface during irradiation significantly suppressed UVB-induced corneal oxidative damage. The results of this study provide for the first time important evidence that trehalose applied on the surface of corneas for two weeks following repeated UVB irradiation (312 nm, daily dose 0.5 J/cm2) accelerated corneal healing, restored corneal transparency and suppressed corneal neovascularization. Compared to buffered saline treatment, following which caspase-3, nitrotyrosine, malondialdehyde and urokinase-type plasminogen activator were still strongly expressed in the corneal epithelium two weeks after irradiation and corneal neovascularization was evident, apoptotic cell death was already significantly reduced after one week of trehalose application. The expression of other markers of injury returned to normal levels during two weeks of trehalose treatment. In conclusion, our results show that trehalose accelerated healing of the UVB irradiated cornea, very probably via suppression of hypoxia-response injury. In addition, immunohistochemical results on corneal cryostat sections corresponded with those obtained using corneal impression cytologies, thus confirming that corneal impression cytologies are useful for diagnostic purposes. SN - 1699-5848 UR - https://www.unboundmedicine.com/medline/citation/22763875/Trehalose_treatment_accelerates_the_healing_of_UVB_irradiated_corneas__Comparative_immunohistochemical_studies_on_corneal_cryostat_sections_and_corneal_impression_cytology_ L2 - http://www.hh.um.es/Abstracts/Vol_27/27_8/27_8_1029.htm DB - PRIME DP - Unbound Medicine ER -