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Apical corneal barrier disruption in experimental murine dry eye is abrogated by methylprednisolone and doxycycline.
Invest Ophthalmol Vis Sci. 2006 Jul; 47(7):2847-56.IO

Abstract

PURPOSE

To evaluate the mechanism of apical corneal epithelial barrier disruption in response to experimental ocular surface desiccation and the effects of two anti-inflammatory agents (methylprednisolone and doxycycline) on this process.

METHODS

Experimental dry eye (EDE) was created in C57BL/6 mice, without or with topical therapy, 1% methylprednisolone, 0.025% doxycycline, or physiologic saline solution (PSS) four times per day. Corneal smoothness and Oregon green dextran (OGD) permeability were assessed. Desquamation of and cornified envelope protein (involucrin and small proline-rich protein [SPRR]-2) expression by the corneal epithelium was evaluated by laser scanning confocal microscopy. Levels of cornified envelope proteins mRNA were measured by real-time PCR.

RESULTS

Corneal OGD permeability, surface irregularity, and the number of desquamating apical corneal epithelia significantly increased in EDE. Desiccating stress significantly increased expression of involucrin and SPRR-2 in the corneal epithelia. Treatment of EDE with methylprednisolone or doxycycline reduced corneal permeability to OGD, improved corneal smoothness, and decreased involucrin and SPRR-2 immunoreactivity compared with EDE+PSS.

CONCLUSIONS

Disruption of apical corneal epithelial barrier function in dry eye is accompanied by increased apical desquamation and increased expression of cornified envelope proteins. Topical treatment of EDE with the anti-inflammatory agents methylprednisolone or doxycycline preserves apical corneal barrier function.

Authors+Show Affiliations

Ocular Surface Center, Department of Ophthalmology, Cullen Eye Institute, Baylor College of Medicine, Houston, Texas 77030, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16799024

Citation

De Paiva, Cintia S., et al. "Apical Corneal Barrier Disruption in Experimental Murine Dry Eye Is Abrogated By Methylprednisolone and Doxycycline." Investigative Ophthalmology & Visual Science, vol. 47, no. 7, 2006, pp. 2847-56.
De Paiva CS, Corrales RM, Villarreal AL, et al. Apical corneal barrier disruption in experimental murine dry eye is abrogated by methylprednisolone and doxycycline. Invest Ophthalmol Vis Sci. 2006;47(7):2847-56.
De Paiva, C. S., Corrales, R. M., Villarreal, A. L., Farley, W., Li, D. Q., Stern, M. E., & Pflugfelder, S. C. (2006). Apical corneal barrier disruption in experimental murine dry eye is abrogated by methylprednisolone and doxycycline. Investigative Ophthalmology & Visual Science, 47(7), 2847-56.
De Paiva CS, et al. Apical Corneal Barrier Disruption in Experimental Murine Dry Eye Is Abrogated By Methylprednisolone and Doxycycline. Invest Ophthalmol Vis Sci. 2006;47(7):2847-56. PubMed PMID: 16799024.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Apical corneal barrier disruption in experimental murine dry eye is abrogated by methylprednisolone and doxycycline. AU - De Paiva,Cintia S, AU - Corrales,Rosa M, AU - Villarreal,Arturo L, AU - Farley,William, AU - Li,De-Quan, AU - Stern,Michael E, AU - Pflugfelder,Stephen C, PY - 2006/6/27/pubmed PY - 2006/8/8/medline PY - 2006/6/27/entrez SP - 2847 EP - 56 JF - Investigative ophthalmology & visual science JO - Invest Ophthalmol Vis Sci VL - 47 IS - 7 N2 - PURPOSE: To evaluate the mechanism of apical corneal epithelial barrier disruption in response to experimental ocular surface desiccation and the effects of two anti-inflammatory agents (methylprednisolone and doxycycline) on this process. METHODS: Experimental dry eye (EDE) was created in C57BL/6 mice, without or with topical therapy, 1% methylprednisolone, 0.025% doxycycline, or physiologic saline solution (PSS) four times per day. Corneal smoothness and Oregon green dextran (OGD) permeability were assessed. Desquamation of and cornified envelope protein (involucrin and small proline-rich protein [SPRR]-2) expression by the corneal epithelium was evaluated by laser scanning confocal microscopy. Levels of cornified envelope proteins mRNA were measured by real-time PCR. RESULTS: Corneal OGD permeability, surface irregularity, and the number of desquamating apical corneal epithelia significantly increased in EDE. Desiccating stress significantly increased expression of involucrin and SPRR-2 in the corneal epithelia. Treatment of EDE with methylprednisolone or doxycycline reduced corneal permeability to OGD, improved corneal smoothness, and decreased involucrin and SPRR-2 immunoreactivity compared with EDE+PSS. CONCLUSIONS: Disruption of apical corneal epithelial barrier function in dry eye is accompanied by increased apical desquamation and increased expression of cornified envelope proteins. Topical treatment of EDE with the anti-inflammatory agents methylprednisolone or doxycycline preserves apical corneal barrier function. SN - 0146-0404 UR - https://www.unboundmedicine.com/medline/citation/16799024/Apical_corneal_barrier_disruption_in_experimental_murine_dry_eye_is_abrogated_by_methylprednisolone_and_doxycycline_ L2 - https://iovs.arvojournals.org/article.aspx?doi=10.1167/iovs.05-1281 DB - PRIME DP - Unbound Medicine ER -