Claudin Expression Modulations Reflect an Injury Response in the Murine Epidermis

The study examined how Claudin (Cldn) expression in the mouse epidermis was modulated during injury and repair induced by TPA. It found that Cldn1 was downregulated and relocated from the membrane to the cytoplasm and nucleus, indicating a mechanism for tight junction modulation during injury. The epidermis experienced thickening and disorganization from 12 to 72 hours post-TPA application, with repair beginning at 96 hours. The study suggested that protein kinase C played a role in these processes, though the exact molecular mechanisms were unclear. Additionally, the research proposed that Cldn1's potential nuclear translocation and interaction with other proteins might influence cell proliferation and differentiation during the injury response.