David T. Woodley

ORCID: 0000-0001-6103-7120
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About
Contact & Profiles
Research Areas
  • Skin and Cellular Biology Research
  • Autoimmune Bullous Skin Diseases
  • Wound Healing and Treatments
  • Cell Adhesion Molecules Research
  • Cellular Mechanics and Interactions
  • Coagulation, Bradykinin, Polyphosphates, and Angioedema
  • Heat shock proteins research
  • Urticaria and Related Conditions
  • Dermatological and Skeletal Disorders
  • Protease and Inhibitor Mechanisms
  • Nail Diseases and Treatments
  • Silk-based biomaterials and applications
  • Tendon Structure and Treatment
  • Bee Products Chemical Analysis
  • Platelet Disorders and Treatments
  • Dermatologic Treatments and Research
  • ATP Synthase and ATPases Research
  • Skin Protection and Aging
  • Endoplasmic Reticulum Stress and Disease
  • Collagen: Extraction and Characterization
  • Corneal Surgery and Treatments
  • Contact Dermatitis and Allergies
  • Cancer, Hypoxia, and Metabolism
  • Cutaneous Melanoma Detection and Management
  • Surgical Sutures and Adhesives

University of Southern California
2015-2024

USC Norris Comprehensive Cancer Center
2003-2024

West Los Angeles College
2014

Southern California University for Professional Studies
2003-2013

Keck Hospital of USC
2006-2010

NHS Blood and Transplant
2010

VA Greater Los Angeles Healthcare System
2004-2009

United States Department of Veterans Affairs
2003-2007

Medical College of Wisconsin
2004

Georgetown University Medical Center
2002

Recessive dystrophic epidermolysis bullosa is an incurable, often fatal mucocutaneous blistering disease caused by mutations in COL7A1, the gene encoding type VII collagen (C7). On basis of preclinical data showing biochemical correction and prolonged survival col7 −/− mice, we hypothesized that allogeneic marrow contains stem cells capable ameliorating manifestations recessive humans.Between October 2007 August 2009, treated seven children who had with immunomyeloablative chemotherapy...

10.1056/nejmoa0910501 article EN New England Journal of Medicine 2010-08-11

Jump-starting and subsequently maintaining epidermal dermal cell migration are essential processes for skin wound healing.These events often disrupted in nonhealing wounds, causing patient morbidity even fatality.Currently available treatments unsatisfactory.To identify novel wound-healing targets, we investigated secreted molecules from transforming growth factor ␣ (TGF␣)-stimulated human keratinoytes, which contained strong motogenic, but not mitogenic, activity.Protein purification...

10.1128/mcb.01287-07 article EN Molecular and Cellular Biology 2008-03-11

A human keratinocyte cDNA expression library in bacteriophage lambda gt11 was screened with the purified IgG fraction of serum from a patient epidermolysis bullosa acquisita, which had high titer anti-type VII collagen antibodies. Screening approximately 3 x 10(5) plaques identified 8 positive clones, largest one (K-131) being 1.9 kilobases size. Dideoxynucleotide sequencing K-131 indicated that it consisted 1875 base pairs and contained an open reading frame coding for putative N-terminal...

10.1073/pnas.88.16.6931 article EN Proceedings of the National Academy of Sciences 1991-08-15

We studied epidermal autografts placed on four severely burned patients. All of the patients experienced skin fragility in autograft sites, and three reported spontaneous blisters. Epidermal-dermal adherence was objectively examined one patient by comparing suction blistering times a parallel, control, unburned site. Blisters formed at 17 minutes, cleavage plane blister below lamina densa basement membrane. In contrast, normal blistered 65 minutes had superficial plane, above basal lamina....

10.1001/jama.1988.03720170042031 article EN JAMA 1988-05-06

10.1016/0304-4165(83)90077-6 article EN Biochimica et Biophysica Acta (BBA) - General Subjects 1983-12-27

Cell migration is a rate-limiting event in skin wound healing. In unwounded skin, cells are nourished by plasma. When wounded, resident encounter serum for the first time. As heals, experience transition of back to this study, we report that human selectively promotes epidermal cell and halts dermal migration. contrast, plasma but not The on-and-off switch operated transforming growth factor (TGF) beta3 levels, which undetectable high serum, TGFbeta receptor (TbetaR) type II low cells....

10.1083/jcb.200507111 article EN The Journal of Cell Biology 2006-03-20

10.1016/j.jaad.2014.04.053 article EN Journal of the American Academy of Dermatology 2014-06-20

10.1111/1523-1747.ep12276531 article EN publisher-specific-oa Journal of Investigative Dermatology 1985-08-01

Wounds that fail to heal in a timely manner, for example, diabetic foot ulcers, pose health, economic, and social problem worldwide. For decades, conventional wisdom has pointed growth factors as the main driving force of wound healing; thus, have become center therapeutic developments. To date, becaplermin (recombinant human PDGF-BB) is only US FDA-approved factor therapy, it shows modest efficacy, costly, potential cause cancer patients. Other molecules drive healing therefore been sought....

10.1172/jci46475 article EN Journal of Clinical Investigation 2011-10-24

Recessive dystrophic epidermolysis bullosa (RDEB) is an incurable disease caused by mutations in the gene encoding type VII collagen, major component of anchoring fibrils (AF). We previously demonstrated that gentamicin produced functional collagen RDEB cells harboring nonsense mutations. Herein, we determined whether topical or intradermal administration induces and AFs patients.A double-blind, placebo-controlled pilot trial assessed safety efficacy 5 patients with The arm tested 0.1%...

10.1172/jci92707 article EN Journal of Clinical Investigation 2017-07-09
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