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Reduced intraepithelial corneal nerve density and sensitivity accompany desiccating stress and aging in C57BL/6 mice.
Exp Eye Res. 2018 04; 169:91-98.EE

Abstract

Dry Eye disease causes discomfort and pain in millions of patients. Using a mouse acute desiccating stress (DS) model we show that DS induces a reduction in intraepithelial corneal nerve (ICN) density, corneal sensitivity, and apical extension of the intraepithelial nerve terminals (INTs) that branch from the subbasal nerves (SBNs). Topical application of 0.02% Mitomycin C (MMC) or vehicle alone has no impact on the overall loss of axon density due to acute DS. Chronic dry eye, which develops progressively as C57BL/6 mice age, is accompanied by significant loss of the ICNs and corneal sensitivity between 2 and 24 months of age. QPCR studies show that mRNAs for several proteins that regulate axon growth and extension are reduced in corneal epithelial cells by 24 months of age but those that regulate phagocytosis and autophagy are not altered. Taken together, these data demonstrate that dry eye disease is accompanied by alterations in intraepithelial sensory nerve morphology and function and by reduced expression in corneal epithelial cells of mRNAs encoding genes mediating axon extension. Précis: Acute and chronic mouse models of dry eye disease are used to evaluate the pathologic effects of dry eye on the intraepithelial corneal nerves (ICNs) and corneal epithelial cells. Data show reduced numbers of sensory nerves and alterations in nerve morphology, sensitivity, corneal epithelial cell proliferation, and expression of mRNAs for proteins mediating axon extension accompany the pathology induced by dry eye.

Authors+Show Affiliations

Department of Anatomy and Regenerative Biology, The George Washington University School of Medicine and Health Sciences, Washington DC, USA; Department of Ophthalmology, The George Washington University School of Medicine and Health Sciences, Washington DC, USA. Electronic address: mastepp@gwu.edu.Department of Anatomy and Regenerative Biology, The George Washington University School of Medicine and Health Sciences, Washington DC, USA.Department of Anatomy and Regenerative Biology, The George Washington University School of Medicine and Health Sciences, Washington DC, USA.Department of Anatomy and Regenerative Biology, The George Washington University School of Medicine and Health Sciences, Washington DC, USA.Department of Ophthalmology, Ocular Surface Center, Cullen Eye Institute, Baylor College of Medicine, Houston, TX, USA.Department of Ophthalmology, Ocular Surface Center, Cullen Eye Institute, Baylor College of Medicine, Houston, TX, USA.

Pub Type(s)

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

Language

eng

PubMed ID

29407221

Citation

Stepp, Mary Ann, et al. "Reduced Intraepithelial Corneal Nerve Density and Sensitivity Accompany Desiccating Stress and Aging in C57BL/6 Mice." Experimental Eye Research, vol. 169, 2018, pp. 91-98.
Stepp MA, Pal-Ghosh S, Tadvalkar G, et al. Reduced intraepithelial corneal nerve density and sensitivity accompany desiccating stress and aging in C57BL/6 mice. Exp Eye Res. 2018;169:91-98.
Stepp, M. A., Pal-Ghosh, S., Tadvalkar, G., Williams, A., Pflugfelder, S. C., & de Paiva, C. S. (2018). Reduced intraepithelial corneal nerve density and sensitivity accompany desiccating stress and aging in C57BL/6 mice. Experimental Eye Research, 169, 91-98. https://doi.org/10.1016/j.exer.2018.01.024
Stepp MA, et al. Reduced Intraepithelial Corneal Nerve Density and Sensitivity Accompany Desiccating Stress and Aging in C57BL/6 Mice. Exp Eye Res. 2018;169:91-98. PubMed PMID: 29407221.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reduced intraepithelial corneal nerve density and sensitivity accompany desiccating stress and aging in C57BL/6 mice. AU - Stepp,Mary Ann, AU - Pal-Ghosh,Sonali, AU - Tadvalkar,Gauri, AU - Williams,Alexa, AU - Pflugfelder,Stephen C, AU - de Paiva,Cintia S, Y1 - 2018/01/31/ PY - 2017/11/29/received PY - 2018/01/25/revised PY - 2018/01/29/accepted PY - 2018/2/7/pubmed PY - 2018/11/14/medline PY - 2018/2/7/entrez KW - Cornea KW - Desiccating stress KW - Dry eye disease KW - Mouse KW - Nerves SP - 91 EP - 98 JF - Experimental eye research JO - Exp Eye Res VL - 169 N2 - Dry Eye disease causes discomfort and pain in millions of patients. Using a mouse acute desiccating stress (DS) model we show that DS induces a reduction in intraepithelial corneal nerve (ICN) density, corneal sensitivity, and apical extension of the intraepithelial nerve terminals (INTs) that branch from the subbasal nerves (SBNs). Topical application of 0.02% Mitomycin C (MMC) or vehicle alone has no impact on the overall loss of axon density due to acute DS. Chronic dry eye, which develops progressively as C57BL/6 mice age, is accompanied by significant loss of the ICNs and corneal sensitivity between 2 and 24 months of age. QPCR studies show that mRNAs for several proteins that regulate axon growth and extension are reduced in corneal epithelial cells by 24 months of age but those that regulate phagocytosis and autophagy are not altered. Taken together, these data demonstrate that dry eye disease is accompanied by alterations in intraepithelial sensory nerve morphology and function and by reduced expression in corneal epithelial cells of mRNAs encoding genes mediating axon extension. Précis: Acute and chronic mouse models of dry eye disease are used to evaluate the pathologic effects of dry eye on the intraepithelial corneal nerves (ICNs) and corneal epithelial cells. Data show reduced numbers of sensory nerves and alterations in nerve morphology, sensitivity, corneal epithelial cell proliferation, and expression of mRNAs for proteins mediating axon extension accompany the pathology induced by dry eye. SN - 1096-0007 UR - https://www.unboundmedicine.com/medline/citation/29407221/Reduced_intraepithelial_corneal_nerve_density_and_sensitivity_accompany_desiccating_stress_and_aging_in_C57BL/6_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4835(17)30830-8 DB - PRIME DP - Unbound Medicine ER -