Accelerating repaired basement membrane after bevacizumab treatment on alkali-burned mouse cornea

Lee, Koon-Ja; Lee, Ji-Young; Lee, Sung Ho; Choi, Tae Hoon

doi:10.5483/bmbrep.2013.46.4.193

Cited by 12 publications

(6 citation statements)

References 21 publications

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“…22 Indeed, TNF-α inhibition after ocular injury has been shown to improve corneal re-epithelialization, 21,22,25 reduce corneal scarring, improve endothelial cell survival, and prevent the formation of peripheral anterior synechiae. 5,[33][34][35][36][37] In this study, we show that early suppression of corneal NV with anti-VEGF DDS reduces TNF-α expression and CD45 + immune cell infiltration into the cornea, ultimately contributing to long-term improvement in corneal re-epithelialization and stromal wound healing as compared with the sham DDS eyes.…”

Section: Discussionmentioning

confidence: 59%

Microporous Drug Delivery System for Sustained Anti-VEGF Delivery to the Eye

Zhou

Singh

Qian

et al. 2020

Trans. Vis. Sci. Tech.

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To describe a novel microporous drug delivery system (DDS) for sustained antivascular endothelial growth factor (VEGF) delivery to the eye and to evaluate its efficacy in a corneal injury model. Methods: A macro-porous DDS (1.5 × 1.5 × 4 mm) loaded with 2 mg of bevacizumab was implanted subconjunctivally in three Dutch-belted pigmented rabbits after corneal alkali injury (2N NaOH). Three rabbits received sham DDS. Animals were followed for three months and assessed in vivo and ex vivo for corneal neovascularization (NV), epithelial defect, stromal scarring, endothelial cell loss, and expression of angiogenic and inflammatory markers in the cornea and retina. Results: Anti-VEGF DDS treatment led to complete inhibition of superior cornea NV and complete corneal re-epithelialization by day 58 whereas sham DDS resulted in severe cornea NV and persistent epithelial defect (9%∼12% of total cornea area) through the end of the study. Histologically, anti-VEGF DDS significantly reduced CD45 + and F4/80 CD11b + cell accumulation (79%, P < 0.05) in the cornea, ameliorated tumor necrosis factor-α expression (90%, P < 0.05), reduced corneal stromal scarring and prevented corneal endothelial cell loss, as compared to sham DDS. Moreover, anti-VEGF DDS achieved retinal penetration and reduction in retinal VEGF levels at 3 months. Conclusions: Use of subconjunctival anti-VEGF DDS suppresses cornea NV, inflammation, stromal scarring, prevents endothelial cell loss, and abrogates retinal VEGF upregulation in a rabbit corneal alkali burn model. Moreover, it delivers anti-VEGF antibodies to the retina for three months. This delivery platform could enable antibody therapy of other corneal and retinal vascular pathologies. Translational Relevance: We describe a method for sustained anti-VEGF delivery to the eye for the treatment of ocular injuries.

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Section: Discussionmentioning

confidence: 59%

Microporous Drug Delivery System for Sustained Anti-VEGF Delivery to the Eye

Zhou

Singh

Qian

et al. 2020

Trans. Vis. Sci. Tech.

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“…Researchers have related the burning effect of NaOH to the anion (hydroxyl) group that causes saponification of the fat and lipids, resulting in tissue softening, followed by increasing the penetration ability of the cation chemicals [15] . While other researchers [16,17] attributed the deleterious effect of alkali on cornea to its strong inflammatory reaction which is characterized by cell infiltration and production of proteolytic enzymes, cytokines oxidative derivatives that could cause severe loss of the extracellular matrix.…”

Section: Discussionmentioning

confidence: 99%

A histological and immunohistochemical study of the effect of platelet- rich plasma on a corneal alkali burn in adult male albino rat

Eldin

Ibrahim

Elswaidy

2019

Egyptian Journal of Histology

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Background: Ocular chemical injuries are an emergency that needs immediate and intensive evaluation and treatment. Platelet-rich plasma (PRP) has become a common treatment in the field of ophthalmological surgery. Aim of the study: to evaluate and compare the alleviating effect of a single dose of PRP injection applied either after 2 hours or 48 hours on an alkali-induced corneal burn. Materials and Methods: Thirty adult male albino rats were equally divided into 5 groups; Control, PRP group, alkali-burn group, alkali-burn+ PRP-treated after 2hours group and alkali-burn+ PRP-treated after 48hours group. Corneal specimens were processed for different histological and immunohistochemical techniques. Results: Alkali burnt cornea revealed focal discontinuity and denudation of corneal epithelium alternating with focal disorganization and stratification. Bowman's membrane appeared irregular with focal disruption. The Descemet's membrane appeared thinned out and disrupted. Mononuclear cellular infiltration and invasion with small blood vessels were observed. Upon intervention with PRP after 2hours of alkali-burn, a near normal corneal histological structure was observed. Yet upon intervention with PRP after 48hours of alkali-burn, a disturbed corneal histological structure with vacuolated epithelium and some nuclear changes were detected. A highly significant difference in the immunohistochemical staining for detection of P53, Ki67, MMP-1 and MMP-9 was detected upon alkali burn compared to the control, whereas a non-significant difference was observed in group IV compared to the control group, yet a significant difference was detected between group V and the control group. Conclusion:A single dose PRP injection had an effective alleviating effect on alkali-induced corneal burn, yet the PRP injection after 2hours of the burn was more efficient in restoring the corneal healthy surface rather than its application after 48 hours.

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“…As a result, it has evolved an efficient system of rapidly resurfacing epithelial defects to avoid microbial infection and further trauma to the underlying stroma (Lee et al, 2013). Migration of the epithelial sheet over the denuded surface and enhanced epithelial cell proliferation, promotes rapid re-epithelialization and the re-establishment of epithelial stratification (Saika et al, 2004a); however, deeper corneal wounds interfere with the proper healing process and result in recurrent corneal erosions, stromal haze, subepithelial fibrosis and epithelial keratinization that may lead to severe visual impairment (Kawashima et al, 2010; Lee et al, 2013). In fact, corneal opacification is the third leading cause of worldwide blindness in the working age population (Foster and Resnikoff, 2005).…”

Section: Corneal Fibrotic Diseasementioning

confidence: 99%

Myofibroblast transdifferentiation: The dark force in ocular wound healing and fibrosis

Shu

Lovicu

2017

Progress in Retinal and Eye Research

284

239

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Wound healing is one of the most complex biological processes to occur in life. Repair of tissue following injury involves dynamic interactions between multiple cell types, growth factors, inflammatory mediators and components of the extracellular matrix (ECM). Aberrant and uncontrolled wound healing leads to a non-functional mass of fibrotic tissue. In the eye, fibrotic disease disrupts the normally transparent ocular tissues resulting in irreversible loss of vision. A common feature in fibrotic eye disease is the transdifferentiation of cells into myofibroblasts that can occur through a process known as epithelial-mesenchymal transition (EMT). Myofibroblasts rapidly produce excessive amounts of ECM and exert tractional forces across the ECM, resulting in the distortion of tissue architecture. Transforming growth factor-beta (TGFβ) plays a major role in myofibroblast transdifferentiation and has been implicated in numerous fibrotic eye diseases including corneal opacification, pterygium, anterior subcapsular cataract, posterior capsular opacification, proliferative vitreoretinopathy, fibrovascular membrane formation associated with proliferative diabetic retinopathy, submacular fibrosis, glaucoma and orbital fibrosis. This review serves to introduce the pathological functions of the myofibroblast in fibrotic eye disease. We also highlight recent developments in elucidating the multiple signaling pathways involved in fibrogenesis that may be exploited in the development of novel anti-fibrotic therapies to reduce ocular morbidity due to scarring.

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Accelerating repaired basement membrane after bevacizumab treatment on alkali-burned mouse cornea

Cited by 12 publications

References 21 publications

Microporous Drug Delivery System for Sustained Anti-VEGF Delivery to the Eye

Microporous Drug Delivery System for Sustained Anti-VEGF Delivery to the Eye

A histological and immunohistochemical study of the effect of platelet- rich plasma on a corneal alkali burn in adult male albino rat

Myofibroblast transdifferentiation: The dark force in ocular wound healing and fibrosis

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