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Sustained Release of TPCA-1 from Silk Fibroin Hydrogels Preserves Keratocyte Phenotype and Promotes Corneal Regeneration by Inhibiting Interleukin-1β Signaling
Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB), Anatomy. School of Medicine, Southeast University, Nanjing , China; Jiangsu Key Laboratory for Biomaterials and Devices, Southeast University, Nanjing , China.ORCID iD: 0000-0003-2700-6739
Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB), Anatomy. School of Medicine, Southeast University, Nanjing , China; Jiangsu Key Laboratory for Biomaterials and Devices, Southeast University, Nanjing , China.
Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB), Anatomy.ORCID iD: 0000-0002-6091-3982
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2020 (English)In: Advanced Healthcare Materials, ISSN 2192-2640, E-ISSN 2192-2659, Vol. 9, no 17, article id 2000591Article in journal (Refereed) Published
Abstract [en]

Corneal injury due to ocular trauma or infection is one of the most challenging vision impairing pathologies that exists. Many studies focus on the pro-inflammatory and pro-angiogenic effects of interleukin-1 beta(IL-1 beta) on corneal wound healing. However, the effect of IL-1 beta on keratocyte phenotype and corneal repair, as well as the underlying mechanisms, is not clear. This study reports, for the first time, that IL-1 beta induces phenotype changes of keratocytes in vitro, by significantly down-regulating the gene and protein expression levels of keratocyte markers (Keratocan, Lumican, Aldh3a1 and CD34). Furthermore, it is found that the NF-kappa B pathway is involved in the IL-1 beta-induced changes of keratocyte phenotype, and that the selective IKK beta inhibitor TPCA-1, which inhibits NF-kappa B, can preserve keratocyte phenotype under IL-1 beta simulated pathological conditions in vitro. By using a murine model of corneal injury, it is shown that sustained release of TPCA-1 from degradable silk fibroin hydrogels accelerates corneal wound healing, improves corneal transparency, enhances the expression of keratocyte markers, and supports the regeneration of well-organized epithelium and stroma. These findings provide insights not only into the pathophysiological mechanisms of corneal wound healing, but also into the potential development of new treatments for patients with corneal injuries.

Place, publisher, year, edition, pages
Wiley-VCH Verlagsgesellschaft, 2020. Vol. 9, no 17, article id 2000591
Keywords [en]
corneal regeneration, interleukin-1 beta, keratocyte, NF-kappa B signaling, silk fibroin
National Category
Ophthalmology
Identifiers
URN: urn:nbn:se:umu:diva-174033DOI: 10.1002/adhm.202000591ISI: 000554483600001PubMedID: 32743953Scopus ID: 2-s2.0-85088834694OAI: oai:DiVA.org:umu-174033DiVA, id: diva2:1458148
Available from: 2020-08-14 Created: 2020-08-14 Last updated: 2023-03-24Bibliographically approved

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Zhang, WeiChen, JialinBackman, Ludvig J.Danielson, Patrik

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