SETD2 epidermal deficiency promotes cutaneous wound healing via activation of AKT/mTOR Signalling.

ABSTRACT:

Objectives

Cutaneous wound healing is one of the major medical problems worldwide. Epigenetic modifiers have been identified as important players in skin development, homeostasis and wound repair. SET domain-containing 2 (SETD2) is the only known histone H3K36 tri-methylase; however, its role in skin wound healing remains unclear.

Materials and methods

To elucidate the biological role of SETD2 in wound healing, conditional gene targeting was used to generate epidermis-specific Setd2-deficient mice. Wound-healing experiments were performed on the backs of mice, and injured skin tissues were collected and analysed by haematoxylin and eosin (H&E) and immunohistochemical staining. In vitro, CCK8 and scratch wound-healing assays were performed on Setd2-knockdown and Setd2-overexp

SUBMITTER: Li X 

PROVIDER: S-EPMC8168411 | biostudies-literature | 2021 Jun

REPOSITORIES: biostudies-literature