"Identification of Protein Directly Affecting Severity of Atopic Dermatitis"

Yonsei University College of Medicine Professors Nam Gitaek and Park Changwook's Team
Atopic Patients Show Decreased 'RAB25' Leading to Reduced Skin Moisture Retention
Provides Clues for Developing Atopic Dermatitis Drugs

[Asia Economy Reporter Lee Gwan-joo] A study has revealed the relationship between the expression level of proteins involved in intracellular material transport and the progression of atopic dermatitis severity. This is expected to serve as a mechanism for atopic dermatitis treatment drugs.

The research team led by Nam Ki-taek from the Department of Biomedical Sciences and Professor Park Chang-wook from the Department of Dermatology at Yonsei University College of Medicine announced on the 21st that a deficiency of the 'RAB25' protein inhibits the formation of keratohyalin granules involved in skin moisturization, reducing the moisturizing factor called 'filaggrin' and worsening atopic dermatitis.

Pro-filaggrin matures into filaggrin within keratohyalin granules, which are protein clusters forming the skin, producing moisturizing factors. Previously, the research team confirmed that a deficiency of the RAB25 protein causes moisture loss in the skin during their studies on skin hydration, and subsequently conducted research to understand the effect and mechanism of RAB25 protein expression on filaggrin production.

The study results showed that the expression level of the RAB25 protein directly affected the severity of atopic dermatitis. It was confirmed that the RAB25 protein promotes cell motility, assisting the maturation process of pro-filaggrin into filaggrin within keratohyalin granules, thereby enhancing skin moisturization.

When RAB25 is deficient, cell motility decreases, inhibiting the growth of keratohyalin granules. This leads to negative effects on skin hydration and other functions. [Source=Yonsei Medical Center]

The research team also compared and analyzed the protein expression levels in normal skin and atopic dermatitis cells to clarify the impact of the RAB25 protein on the skin. The expression level of the RAB25 protein in atopic dermatitis was significantly lower, at 1/36 of that in normal skin samples. This demonstrated that a deficiency of the RAB25 protein increases the severity of atopic dermatitis.

Furthermore, the team conducted drug validation in animal experiments and suggested directions for developing atopic dermatitis treatment drugs. After injecting Calpeptin, which restores skin cells, into mice lacking the RAB25 protein and observing the progress, they confirmed that cell motility increased, filaggrin expression rose, and atopic dermatitis symptoms improved.

Professor Nam stated, "We were able to understand the process of improving skin moisturization by elucidating that a deficiency of the RAB25 protein increases the severity of atopic dermatitis and clarifying the maturation mechanism of filaggrin. Through the treatment drug mechanism discovered in this study, we will continue research to overcome atopic dermatitis in the future."

The results of this study were published in the latest issue of the leading international journal in the field of allergy immunology, Allergy (IF 14.710).

This content was produced with the assistance of AI translation services.