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Updated: Apr 14, 2026

Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin
Published on: July 14, 2017
Barrier Function of the Repaired Skin Is Disrupted Following Arrest of Dicer in Keratinocytes
Subhadip Ghatak1, Yuk Cheung Chan1, Savita Khanna1
1Department of Surgery, Davis Heart and Lung Research Institute, Center for Regenerative Medicine and Cell-Based Therapies, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA.
Abstract:
Tissue injury transiently silences miRNA-dependent posttranscriptional gene silencing in its effort to unleash adult tissue repair. Once the wound is closed, miRNA biogenesis is induced averting neoplasia. In this work, we report that Dicer plays an important role in reestablishing the barrier function of the skin post-wounding via a miRNA-dependent mechanism. MicroRNA expression profiling of skin and wound-edge tissue revealed global upregulation of miRNAs following wound closure at day 14 post-wounding with significant induction of Dicer expression. Barrier function of the skin, as measured by trans-epidermal water loss, was compromised in keratinocyte-specific conditional (K14/Lox-Cre) Dicer-ablated mice because of malformed cornified epithelium lacking loricrin expression. Studies on human keratinocytes recognized that loricrin expression was inversely related to the expression of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1). Compared to healthy epidermis, wound-edge keratinocytes from Dicer-ablated skin epidermis revealed elevated p21(Waf1/Cip1) expression. Adenoviral and pharmacological suppression of p21(Waf1/Cip1) in keratinocyte-specific conditional Dicer-ablated mice improved wound healing indicating a role of Dicer in the suppression of p21(Waf1/Cip1). This work upholds p21(Waf1/Cip1) as a druggable target to restore barrier function of skin suffering from loss of Dicer function as would be expected in diabetes and other forms of oxidant insult.
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