Mary C. Williams, Ph.D.

Faculty and Fellows

Professor of Medicine
Associate Director, Pulmonary Center

Undergraduate Education: University of Illinois, Urbana
Graduate School: University of California, San Francisco, PhD, 1971
Thesis title: Permeability of Intestinal and Diaphragmmatic Capillaries to Protein Tracers of Large Molecular Weight
Post-doctoral Fellowships: Cardiovascular Research Center, University of California, San Francisco

Special Interests:

  • Alveolar epithelial cell biology and development
  • Regulation of alveolar type I cell phenotype and gene expression
  • Molecular mechanisms of alveolar repair

Dr. Williams is Professor of Medicine in the Departments of Medicine and Anatomy. She is the prinicipal investigator of a Program Project Grant in lung development entitiled Regulation of Alveolar Epithelial Cell Differentiation that has been funded continuously since 1991. Work in Dr. Williams’ laboratory is centered on molecular studies of the alveolar type I cell, the cell that forms the extensive gas exchange surface of the peripheral lung. Current studies make use of cell and molecular techniques to understand how type I cells form during development, how these cells are replaced after an injuries such as hyperoxia, the role of type I cells and type I cell genes in lung adenocarcinoma progression, and others.

Selected Publications:

  1. Millien G, Hinds A, Wang J, Williams MC, and Ramirez MI. Progressive alterations in alveolus formation and gene expression in T1a null mutant lungs link epithelial type I cell morphogenesis to inhibition of distal cell proliferation. Submitted
  2. Cao YX, Hinds A, Ramirez MI, and Williams MC. The 10kb T1alpha promoter drives cell-specific expression in normal tissue sites including alveolar type I cells, lymphatics, and brain ependymal cells. Submitted
  3. Kathuria H, Cao YX, Ramirez MI, and Williams MC. Transcription of the caveolin-1 gene is differentially regulated in lung type I epithelial and endothelial cell lines: Role for Ets transcription factors in epithelial cell expression. J. Biol. Chem. 279:30028-30036, 2004
  4. Cao, Y.X., M.I. Ramirez, and M.C. Williams. Enhanced binding of Sp1/Sp3 transcription factors mediates the hyperoxia-induced increased expression of the lung type I cell gene T1?. J. Cell. Biochem. 89:887-901, 2003.
  5. Ramirez, M. I., G. Millien, A. Hinds, YX Cao, D. C. Seldin, and M. C. Williams. T1?, a lung type I cell differentiation gene, is required for normal lung cell proliferation and alveolus formation at birth. Dev. Biol. 256:61-72, 2003.
  6. Schacht, V., M. I. Ramirez, Y-K. Hong, S. Hirakawa, D. Feng, N. Harvey, M. C. Williams, A. M. Dvorak, H. F. Dvorak, G. Oliver, and M. Detmar. T1?/podoplanin deficiency disrupts normal lymphatic vascular formation and causes lymphedema. EMBO Journal, 22:3546-3556, 2003.
  7. Williams, M. C. Alveolar type I cells: Molecular phenotype and development. Ann. Rev. Physiol. 65:669-695. 2003

Selected Reprints:

  1. T1alpha, a lung type I cell differentiation gene, is required for normal lung cell proliferation and alveolus formation at birth
  2. Transcription of the Caveolin-1 Gene Is Differentially Regulated in Lung Type I Epithelial and Endothelial Cell Lines
  3. Enhanced Binding of Sp1/Sp3 Transcription Factors Mediates the Hyperoxia-Induced Increased Expression of the Lung Type I Cell Gene T1a

Awards and Honors:

  • American Thoracic Society Award for Scientific Accomplishments (2000)
  • American Thoracic Society Task Force on Women, ‘for pioneering efforts’ (1999)
  • American Thoracic Society Presidential Commendation as founding journal editor of American Journal of Respiratory Cell and Molecular Biology (1993)
  • Kaiser Award for Excellence in Teaching (1976)
  • University of California San Francisco Regent’s Fellow (1966-69)
  • Phi Beta Kappa, Phi Kappa Phi (1955)