SOX9 in Keratinocytes Regulates Claudin 2 Transcription during Skin Aging

Abstract

In order to prove that SOX9 in keratinocytes regulates claudin 2 transcription during skin aging, the skin of 8-week-old and 24-month-old mice is sequenced to obtain a differentially expressed gene SOX9. The gene is mainly expressed in keratinocytes, and it increases first and then decreases from newborn to aging. Six core sequences of SOX9 and claudin 2 are predicted from Jaspar. The double Luciferase Report shows that overexpression of SOX9 induces the full-length promoter of claudin 2 significantly and has no effect on the mutation and cleavage plasmid without SOX9 response. Claudin 2 is consistent with SOX9 in the skin of mice of different ages, and SOX9 is strongly positively correlated with claudin 2. Finally, overexpression of SOX9 and claudin 2 will delay PM2.5-induced keratinocyte senescence. The silencing of claudin 2 leads to the loss of SOX9 function. It is clearly evident that SOX9 can affect the transcription of claudin 2, which increases first and then decreases in the process of mice from newborn to aging. SOX9 inhibits proinflammatory mediators, increases antioxidant capacity, and restores keratin differentiation. It can effectively prevent melanin deposition and delay aging.

Marine Bioactive Peptides: Anti-Photoaging Mechanisms and Potential Skin Protective Effects

“…Oxidative stress, characterized by an imbalance between oxidation and antioxidant mechanisms within the body, constitutes a significant contributor to skin photoaging [58,59] (Figure 2). In the context of normal physiological conditions, a limited quantity of reactive oxygen species (ROS) exerts an immune defense effect and confers benefits to the body [60] (Table 1).…”