Effects of topical chondrocyte‑derived extracellular matrix treatment on corneal wound healing, following an alkali burn injury

Yang,Jae‑Wook; Lee,Soung‑Min; Oh,Kyeong‑Hee; Park,Sae‑Gwang; Choi,Ii‑Whan; Seo,Su‑Kil

doi:10.3892/mmr.2014.2722

Effects of topical chondrocyte‑derived extracellular matrix treatment on corneal wound healing, following an alkali burn injury

Authors:
- Jae‑Wook Yang
- Soung‑Min Lee
- Kyeong‑Hee Oh
- Sae‑Gwang Park
- Ii‑Whan Choi
- Su‑Kil Seo
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Affiliations: Department of Ophthalmology, Busan Paik Hospital, Inje University, Busan 614‑735, Republic of Korea, Ocular Neovascular Research Center, College of Medicine, Inje University, Busan 614‑735, Republic of Korea
Published online on: October 21, 2014 https://doi.org/10.3892/mmr.2014.2722
Pages: 461-467

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Abstract

Numerous treatments have been used in the management of corneal chemical burns; however, no optimal treatment for corneal chemical burns currently exists. The present study investigated the effects of topical chondrocyte‑derived extracellular matrix (CD‑ECM) treatment on corneal wound healing, using an alkali burn mouse model. Topical treatment with CD‑ECM was shown to reduce corneal opacity following an alkali burn. A histological examination observed the presence of regenerated epithelial cells and a small number of inflammatory cells in the corneas of CD‑ECM‑treated mice. The majority of the inflammatory cells present in the corneas of the phosphate‑buffered saline (PBS)‑treated mice were neutrophils that expressed matrix metalloproteinase (MMP)‑9. The amount of neutrophils was significantly reduced in the corneas of the CD‑ECM‑treated mice. Furthermore, the expression levels of interleukin (IL)‑8 were significantly reduced in the CD‑ECM treatment group, but not in the mice that received the PBS treatment. The results of the present study indicate that CD‑ECM treatment may accelerate wound healing in a model of alkali burn‑induced corneal injury. The therapeutic mechanism may be associated with accelerated reepithelialization and reduced recruitment of MMP‑9‑expressing neutrophils, through inhibiting the production of IL‑8.

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