Improving Wound Healing with DICER1-Modified Keratinocytes.

ABSTRACT: Wound healing is a complex, orchestrated process, and impaired wound closure, as seen in diverse pathological states, occurs due to interference during this dynamic process. Here, we show that DICER1 levels that are downregulated in stalled wounds during diabetes promote effective wound closure when they are upregulated. Using Lipofectamine 2000, HaCaT cells were transfected with either the empty vector or the Dicer1 overexpression plasmid, and after 24 and 48 h, there was increased wound closure by Dicer1 overexpression as compared to only vector-transfected cells, and this was accompanied by the upregulation of wound-healing genes. Since Lipofectamine 2000 exerts significant cell toxicity, we employed a more specific and comparatively less toxic in-house-developed cell-penetrating peptid

SUBMITTER: Choudhury SG 

PROVIDER: S-EPMC12461399 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature