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Tongyu Cao Wikramanayake, Ph.D.

Dermatology and Cutaneous Surgery
University of Miami Miller School of Medicine
1600 NW 10th Avenue
RMSB 2023A
Miami, FL 33136

Phone: 305-243-8878 Fax: 304-243-2200 Email
Understanding the mechanisms regulating the differentiation of skin structures and appendages (e.g., hair follicle, sebaceous gland) is critical for developing more targeted and effective therapies for various skin and hair disorders, such as alopecia, sebaceous gland dysfunction, barrier defects, inflammatory skin disorders, and non-healing wounds.

Lately, we have generated Mpzl3 (Myelin Protein Zero-like 3) knockout mice that develop a variety of abnormalities that mimic human skin and hair disorders. The MPZL3 protein has been shown to be an essential regulator of epidermal terminal differentiation, and is highly conserved between human and mouse. Therefore, we are using these mice as a model system to understand the pathobiology of these disorders and to develop novel therapeutic approaches.

The role of MPZL3 in epidermal barrier structure and function

The epidermis functions as an effective barrier that prevents dehydration from the loss of body water, poisoning from the absorption of noxious substances, and systemic infection from surface microorganisms. Mpzl3 knockout mice show defective epidermal barrier function with increased permeability and spontaneous skin inflammation. Understanding how MPZL3 regulates barrier formation will provide novel targets to treat barrier defects.

The role of MPZL3 in sebaceous gland function

Sebaceous gland dysfunction is the cause of some very common skin disorders such as acne, sebaceous hyperplasia, and seborrheic dermatitis. Mpzl3 knockout mice show sebaceous hyperplasia, oily skin, and seborrheic dermatitis-like skin inflammation. Understanding how MPZL3 regulates sebaceous differentiation may provide novel approaches to treat these disorders.

The role of MPZL3 in hair follicle function

The hair follicles go through cycles of regeneration after birth, and many common alopecia (hair loss) disorders are caused by abnormal hair follicle cycling. We are using transgenic and knockout mouse models to understand the molecular basis of hair cycle regulation in order to discover new ways to prevent and treat different alopecia disorders.

We also collaborate with other investigators in wound healing research. Chronic wounds, such as diabetic foot ulcers, venous leg ulcers and pressure (bed) ulcers, are the leading cause of lower-leg amputations in the elderly and in people with diabetes. We are using mouse models with wound healing defects to test novel therapeutics for chronic wounds.