Sustained Release of TPCA‐1 from Silk Fibroin Hydrogels Preserves Keratocyte Phenotype and Promotes Corneal Regeneration by Inhibiting Interleukin‐1 β Signaling

Abstract: 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‐1β (IL‐1β) on corneal wound healing. However, the effect of IL‐1β on keratocyte phenotype and corneal repair, as well as the underlying mechanisms, is not clear. This study reports, for the first time, that IL‐1β 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‐κB pathway is involved in the IL‐1β‐induced changes of keratocyte phenotype, and that the selective IKKβ inhibitor TPCA‐1, which inhibits NF‐κB, can preserve keratocyte phenotype under IL‐1β 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.

Angaben zum Objekt

• Standort: Deutsche Nationalbibliothek Frankfurt am Main
• Umfang: Online-Ressource
• Sprache: Englisch

Verweise und Beziehungen

• Erschienen in: Sustained Release of TPCA‐1 from Silk Fibroin Hydrogels Preserves Keratocyte Phenotype and Promotes Corneal Regeneration by Inhibiting Interleukin‐1 β Signaling ; volume:9 ; number:17 ; year:2020 ; extent:14 ; Advanced healthcare materials ; 9, Heft 17 (2020) (gesamt 14)

Beteiligte, Orts- und Zeitangaben

• Urheber: Zhang, Wei ; Chen, Jialin ; Qu, Mingli ; Backman, Ludvig J. ; Zhang, Aini ; Liu, Haoyang ; Zhang, Xiaoping ; Zhou, Qingjun ; Danielson, Patrik

Weitere Informationen

• DOI: 10.1002/adhm.202000591
• URN: urn:nbn:de:101:1-2022062309080336128011
• Rechteinformation: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
• Letzte Aktualisierung: 15.08.2025, 07:20 MESZ