Mei Chen, PhD

Professor of Dermatology

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Overview

Dr. Chen obtained a Ph.D. in Cell Biology, Virology and Molecular Biology at Albert Einstein College of Medicine in New York. After postdoctoral training in Cell and Developmental Biology at Memorial Sloan-Kettering Cancer Center and Cornell University Medical College, Dr. Chen joined the faculty of the department of Dermatology at Northwestern University Medical School, followed by an appointment at the University of Southern California where she is currently Professor and Director of USC Laboratories for Investigative Dermatology. Dr. Chen’s research has focused on elucidating the structure and function of type VII (anchoring fibril) collagen and developing various therapeutic approaches including cell therapy, small molecule-based drug therapy, protein therapy and gene therapy for the treatment of recessive dystrophic epidermolysis bullosa (RDEB). Her current research plans are 1) to evaluate the effects of recombinant type VII collagen (rC7) on skin wounds in normal and diabetic pigs. This is because it is known that pigskin is the most similar of all species to human skin. This will provide essential data for moving rC7 from the laboratory bench to the patient’s bedside; 2) To determine the signaling pathway(s) responsible for RDEB scarring and identify the mechanism(s) by which rC7 inhibits skin wound scar formation; this work may lead to insights into the pathology of scars and identifiable targets for agents to prevent skin scarring; 3) To evaluate aminoglycoside-based drug therapy for RDEB in human patients; and 4) To identify the changes in RDEB-associated squamous cell carcinoma (SCC) at the cellular and molecular levels and elucidate signaling pathways leading to onset of RDEB SCC that may provide targets for anti-SCC drug development. All of these studies have strong translational potential and will hopefully advance future therapies for patients with RDEB, patients with devastating scarring conditions (burn victims, RDEB patients, keloids, chronic graft-versus-host disease, scleroderma, and others), and patients with chronic non-healing wounds (diabetic ulcers, decubitus ulcers and stasis dermatitis ulcers). The entirety of her work will generate novel insights into cutaneous biology and has great translational potential towards bringing rC7 “from the laboratory bench to the bedside of patients”. Our research programs have been continuously supported by NIH grants for the last twenty years.

Research Funding

  • A Pilot Study of the Effect of Intravenous Gentamicin on the Restoration of Full-Length Type VII Collagen in RDEB Patients Carrying Nonsense Mutations
    NIH · R21AR071716 · Mar 1, 2018 – Feb 28, 2021 · Role: Principal Investigator
  • Protein Therapy for Recessive Dystrophic Epidermolysis Bullosa
    NIH · RC4AR060535 · Sep 20, 2010 – Sep 30, 2013 · Role: Principal Investigator
  • Strategies Towards Gene Therapy for Dystrophic Epidermolysis Bullosa
    NIH · R01AR047981 · Aug 1, 2001 – Jun 30, 2012 · Role: Principal Investigator
  • Purification of Epidermolysis Bullosa Antigen
    NIH · R01AR033625 · Apr 1, 1984 – Aug 31, 2015 · Role: Co-Principal Investigator

Publications

  • A Novel Fully Humanized 3D Skin Equivalent to Model Early Melanoma Invasion. Mol Cancer Ther. 2015 Nov; 14(11):2665-73.. View in PubMed
  • Intravenously Administered Recombinant Human Type VII Collagen Derived from Chinese Hamster Ovary Cells Reverses the Disease Phenotype in Recessive Dystrophic Epidermolysis Bullosa Mice. J Invest Dermatol. 2015 Dec; 135(12):3060-3067.. View in PubMed
  • Reduced Toxicity Conditioning and Allogeneic Hematopoietic Progenitor Cell Transplantation for Recessive Dystrophic Epidermolysis Bullosa. J Pediatr. 2015 Sep; 167(3):765-9.e1.. View in PubMed
  • Recessive Dystrophic Epidermolysis Bullosa: Advances in the Laboratory Leading to New Therapies. J Invest Dermatol. 2015 Jul; 135(7):1705-1707.. View in PubMed
  • Keratinocyte Migration and a Hypothetical New Role for Extracellular Heat Shock Protein 90 Alpha in Orchestrating Skin Wound Healing. Adv Wound Care (New Rochelle). 2015 Apr 01; 4(4):203-212.. View in PubMed
  • Hsp90α and Hsp90β together operate a hypoxia and nutrient paucity stress-response mechanism during wound healing. J Cell Sci. 2015 Apr 15; 128(8):1475-80.. View in PubMed
  • Identification of the critical therapeutic entity in secreted Hsp90α that promotes wound healing in newly re-standardized healthy and diabetic pig models. PLoS One. 2014; 9(12):e113956.. View in PubMed
  • Aminoglycosides restore full-length type VII collagen by overcoming premature termination codons: therapeutic implications for dystrophic epidermolysis bullosa. Mol Ther. 2014 Oct; 22(10):1741-52.. View in PubMed
  • De novo anti-type VII collagen antibodies in patients with recessive dystrophic epidermolysis bullosa. J Invest Dermatol. 2014 Apr; 134(4):1138-1140.. View in PubMed
  • Extracellular heat shock protein 90 signals through subdomain II and the NPVY motif of LRP-1 receptor to Akt1 and Akt2: a circuit essential for promoting skin cell migration in vitro and wound healing in vivo. Mol Cell Biol. 2013 Dec; 33(24):4947-59.. View in PubMed