Modeling the Epidermal Barrier in Atopic Dermatitis with 3D Human Skin Organoids
Session Number
Project ID: BIO 07
Advisor(s)
Dr. Bethany E Perez White; Northwestern University, Feinberg School of Medicine
Discipline
Biology
Start Date
19-4-2023 10:35 AM
End Date
19-4-2023 10:50 AM
Abstract
The epidermal barrier is essential for maintaining skin homeostasis, yet the cellular signaling mechanisms that lead to its formation and function are relatively unknown. Perturbations in the epidermal barrier cause many different skin diseases, including atopic dermatitis. Our investigations will help define signaling mechanisms impacting the barrier in atopic dermatitis using a 3D human skin organoid model made from primary skin cells. To probe these mechanisms, we will determine expression levels of transcripts (mRNA) by quantitative polymerase chain reaction (qPCR). First, we had to ensure that known atopic dermatitis mRNA expression patterns were the same in our model. For example, the barrier protein filaggrin is downregulated in the skin of patients with atopic dermatitis. According to our qPCR data, our results align with patient data. We observed the same loss of filaggrin transcripts in our atopic dermatitis 3D organoid model. These results establish the validity of the model. The long-term goal of our studies is to investigate the potential of re-establishing the balance of signaling mechanisms as possible means of restoring the epidermal barrier and treating atopic dermatitis.
Modeling the Epidermal Barrier in Atopic Dermatitis with 3D Human Skin Organoids
The epidermal barrier is essential for maintaining skin homeostasis, yet the cellular signaling mechanisms that lead to its formation and function are relatively unknown. Perturbations in the epidermal barrier cause many different skin diseases, including atopic dermatitis. Our investigations will help define signaling mechanisms impacting the barrier in atopic dermatitis using a 3D human skin organoid model made from primary skin cells. To probe these mechanisms, we will determine expression levels of transcripts (mRNA) by quantitative polymerase chain reaction (qPCR). First, we had to ensure that known atopic dermatitis mRNA expression patterns were the same in our model. For example, the barrier protein filaggrin is downregulated in the skin of patients with atopic dermatitis. According to our qPCR data, our results align with patient data. We observed the same loss of filaggrin transcripts in our atopic dermatitis 3D organoid model. These results establish the validity of the model. The long-term goal of our studies is to investigate the potential of re-establishing the balance of signaling mechanisms as possible means of restoring the epidermal barrier and treating atopic dermatitis.