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The Dai lab studies the intrinsic and extrinsic control of stem/progenitor cells in normal and diseased epithelial tissues. Skin – largest organ in the human body, is our major tissue of interest. Skin provides an essential physical and immunological barrier for organismal survival and health, and is a leading model for tissue stem cell research. The skin research field is populated by exceptional scientists and high-quality scientific literature, providing an intellectually stimulating ground for scientific interrogation.
Current research focuses on several areas:
- Intrinsic and extrinsic control of stem cell activation.
Our hairs grow and fall out because of the precisely controlled activities of stem cells that reside in the hair follicle. These stem cells are dormant at times but become activated upon proper stimuli to regenerate a new hair follicle that then produces a new hair. We study what genes within the hair follicle stem cells to tell them to become activated, and what cells in the skin tissue microenvironment send signals to control their activity.
Examples:
Sun et al. Pygo2 regulates β-catenin-induced activation of hair follicle stem/progenitor cells and skin hyperplasia. Proc Natl Acad Sci U S A. 2014 Jul 15;111(28):10215-20.
Lee et al. Transcriptional mechanisms link epithelial plasticity to adhesion and differentiation of epidermal progenitor cells. Dev Cell. 2014 Apr 14;29(1):47-58.
- Epithelial-immune interplay that controls barrier function and skin inflammation.
Excessive inflammation causes skin diseases that affect quality of life. Psoriasis and atopic dermatitis are two most common inflammatory skin diseases. Although a role for epidermal cells has been implicated in disease pathogenesis, the precise molecular and cellular mechanisms that regulate disease severity and progression remain to be fully understood. We use mouse disease models to elucidate these mechanisms, and collaborate with dermatologists to study the pathogenesis of human inflammatory skin diseases with unknown pathogenesis using single-cell RNA-sequencing, spatial transcriptomics, and tissue imaging. As commensal microbials are an integral part of the skin microenvironment that comes into direct contact with the epidermis, we also study how commensal bacteria impact the fate of epidermal stem/progenitor cells.
Examples:
Sun et al. OVOL1 Regulates Psoriasis-Like Skin Inflammation and Epidermal Hyperplasia. J Invest Dermatol. 2021 Jun;141(6):1542-1552.
Dragan, Sun et al. Epidermis-Intrinsic Transcription Factor Ovol1 Coordinately Regulates Barrier Maintenance and Neutrophil Accumulation in Psoriasis-Like Inflammation. J Invest Dermatol. 2022 Mar;142(3 Pt A):583-593.e5.
- Understanding and correcting delayed wound healing in aged and diabetic skin.
Cutaneous wound healing is essential to restore barrier function of injured skin. However, healing is often impaired upon aging or in diabetic patients, resulting in chronic wounds. Combining single-cell RNA-sequencing with mouse genetics, we study the steps that epidermal stem/progenitor cells undertake to expand, migrate, and differentiate to make a new epidermis, the molecular mechanism that regulate these cellular events, as well as the changes in cellular compositions, signaling communications, and metabolic processes during pathological wound healing. Our long-term goal is to identify critical circuits that can be therapeutically targeted in order to improve healing.
Examples:
Haensel, Jin et al. Defining Epidermal Basal Cell States during Skin Homeostasis and Wound Healing Using Single-Cell Transcriptomics. Cell Rep. 2020 Mar 17;30(11):3932-3947.e6.
Vu, Jin, Sun et al. Wound healing in aged skin exhibits systems-level alterations in cellular composition and cell-cell communication. Cell Rep. 2022 Aug 2;40(5):111155.