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Article: Experimental modeling of cornea wound healing in diabetes: clinical applications and beyond

TitleExperimental modeling of cornea wound healing in diabetes: clinical applications and beyond
Authors
Keywordsanimal models
diabetes
cornea
epithelial wound healing
immunity
Issue Date2019
PublisherBMJ Publishing Group: Open Access. The Journal's web site is located at http://drc.bmj.com/
Citation
BMJ Open Diabetes Research & Care, 2019, v. 7, p. article no. e000779 How to Cite?
AbstractDiabetes mellitus is the most common cause of blindness in working age populations worldwide. While much of the focus for public health has been on secondary prevention in sight-threatening diabetic retinopathy, the cornea, including its epithelium and nerves, represents a major site of damage by chronic hyperglycemia. On injury, the diabetic cornea exhibits a delayed wound-healing response, as well as an altered ocular surface immune response. This suggests a potential association between the dysfunctional wound healing response and altered inflammation on the ocular surface. However, the presence of potential confounders makes this association difficult to investigate in human epidemiological studies. Thus, we turn to animal diabetic models for a better understanding. In this review, 20 original studies, published between 2008 and 2018, describe in vivo and in vitro models of diabetic cornea disease. We compared different models of diabetic cornea wound healing and discussed the relative strengths and drawbacks of each model. A number of molecular and cellular components involved in the corneal wound healing response that are altered in the presence of diabetes have been identified in the reviewed studies. Particularly, altered corneal epithelial protein concentrations of lumician and occludin were detected in diabetic eyes compared with controls. Additionally, the importance of IL-1β in modulating the inflammatory response after corneal injury in patients with diabetes and controls was further elucidated. Meanwhile, abnormal P2×7 receptor localization and decreased corneal sub-basal nerve density in diabetic eyes were shown to contribute to altered corneal nerve signaling after injury and thus affecting the wound healing response. Finally, the discovery of the therapeutic effects of topically administered aloe vera, Serpine 1, Resolvin D1 (RvD1), pigment epithelium-derived factor (PEDF) and Pro-His-Ser-Arg-Asn in diabetic animal models of cornea epithelial and nerve injury provide encouraging evidence for the future availability of effective treatment for diabetic keratopathy.
Persistent Identifierhttp://hdl.handle.net/10722/279951
ISSN
2018 Impact Factor: 5.067

 

DC FieldValueLanguage
dc.contributor.authorBU, Y-
dc.contributor.authorShih, KC-
dc.contributor.authorKwok, SS-
dc.contributor.authorChan, YK-
dc.contributor.authorLo, ACY-
dc.contributor.authorChan, TCY-
dc.contributor.authorJhanji, V-
dc.contributor.authorTong, L-
dc.date.accessioned2019-12-23T08:24:07Z-
dc.date.available2019-12-23T08:24:07Z-
dc.date.issued2019-
dc.identifier.citationBMJ Open Diabetes Research & Care, 2019, v. 7, p. article no. e000779-
dc.identifier.issn2052-4897-
dc.identifier.urihttp://hdl.handle.net/10722/279951-
dc.description.abstractDiabetes mellitus is the most common cause of blindness in working age populations worldwide. While much of the focus for public health has been on secondary prevention in sight-threatening diabetic retinopathy, the cornea, including its epithelium and nerves, represents a major site of damage by chronic hyperglycemia. On injury, the diabetic cornea exhibits a delayed wound-healing response, as well as an altered ocular surface immune response. This suggests a potential association between the dysfunctional wound healing response and altered inflammation on the ocular surface. However, the presence of potential confounders makes this association difficult to investigate in human epidemiological studies. Thus, we turn to animal diabetic models for a better understanding. In this review, 20 original studies, published between 2008 and 2018, describe in vivo and in vitro models of diabetic cornea disease. We compared different models of diabetic cornea wound healing and discussed the relative strengths and drawbacks of each model. A number of molecular and cellular components involved in the corneal wound healing response that are altered in the presence of diabetes have been identified in the reviewed studies. Particularly, altered corneal epithelial protein concentrations of lumician and occludin were detected in diabetic eyes compared with controls. Additionally, the importance of IL-1β in modulating the inflammatory response after corneal injury in patients with diabetes and controls was further elucidated. Meanwhile, abnormal P2×7 receptor localization and decreased corneal sub-basal nerve density in diabetic eyes were shown to contribute to altered corneal nerve signaling after injury and thus affecting the wound healing response. Finally, the discovery of the therapeutic effects of topically administered aloe vera, Serpine 1, Resolvin D1 (RvD1), pigment epithelium-derived factor (PEDF) and Pro-His-Ser-Arg-Asn in diabetic animal models of cornea epithelial and nerve injury provide encouraging evidence for the future availability of effective treatment for diabetic keratopathy.-
dc.languageeng-
dc.publisherBMJ Publishing Group: Open Access. The Journal's web site is located at http://drc.bmj.com/-
dc.relation.ispartofBMJ Open Diabetes Research & Care-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectanimal models-
dc.subjectdiabetes-
dc.subjectcornea-
dc.subjectepithelial wound healing-
dc.subjectimmunity-
dc.titleExperimental modeling of cornea wound healing in diabetes: clinical applications and beyond-
dc.typeArticle-
dc.identifier.emailShih, KC: kcshih@hku.hk-
dc.identifier.emailChan, YK: josephyk@connect.hku.hk-
dc.identifier.emailLo, ACY: amylo@hku.hk-
dc.identifier.authorityShih, KC=rp01374-
dc.identifier.authorityChan, YK=rp02536-
dc.identifier.authorityLo, ACY=rp00425-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1136/bmjdrc-2019-000779-
dc.identifier.scopuseid_2-s2.0-85075899019-
dc.identifier.hkuros308783-
dc.identifier.volume7-
dc.identifier.spagearticle no. e000779-
dc.identifier.epagearticle no. e000779-
dc.publisher.placeUnited Kingdom-

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