Tushar Desai
Academic Appointments
- Assistant Professor, Medicine - Pulmonary & Critical Care Medicine
Key Documents
Contact Information
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Clinical Offices
Chest Clinic 300 Pasteur Dr A283 MC 5351 Stanford, CA 94305 Tel Work (650) 725-7061 Fax (650) 498-6288
- Academic Offices
Not for medical emergencies or patient use
Professional Overview
Clinical Focus
- Pulmonary Disease
Honors and Awards
- Mentored Clinical Scientist Research Career Development Award (K08), NIH (2008-2013)
- Fellowship in Pulmonary Research, Parker B. Francis Foundation (2006-2009)
- Pulmonary Fellowship Award, GlaxoSmithKline (2002-2003)
- Robert Dawson Evans Fellow Excellence in Teaching Award, Boston University School of Medicine, Department of Internal Medicine (2000)
- House Officer Research Award, University of Michigan Hospitals, Department of Internal Medicine (1998)
- Worth F. Bloom M25 Prize, Tufts University School of Medicine (1995)
Professional Education
| Internship: | University of Michigan Medical Center MI (1996) |
| Residency: | University of Michigan Medical Center MI (1998) |
| Board Certification: | Pulmonary Disease, American Board of Internal Medicine (2001) |
| Fellowship: | Boston University School of Medicine MA (2002) |
| Medical Education: | Tufts University School of Medicine MA (1995) |
| BA: | Amherst College, Psychology (1991) |
Graduate & Fellowship Program Affiliations
Scientific Focus
Current Research Interests
My lab is interested in understanding how alveolar epithelial type (AT) 1 and AT 2 cells are generated during lung development and replaced in adult life during aging and following injury. We use mouse genetic tools to specifically mark and fate-map AT 1 and AT 2 cells, in order to understand their differentiative potential and the lineage hierarchies that operate during alveolar epithelial turnover. By genetically deleting or mis-expressing transcription factors and other genes in AT 1 and AT 2 cells, we are also seeking to elucidate the specific role each gene plays in these cells and indirectly in the lung overall. We are interested not only in the role for AT 1 and AT 2 cells in health, but in exploring how their depletion or dysregulation may contribute to specific diseases, such as adenocarcinoma, emphysema, bronchopulmonary dysplasia, and fibrotic diseases of the lung.
Publications
- In vitro and in vivo gene therapy vector evolution via multispecies interbreeding and retargeting of adeno-associated viruses J Virol. 2008; (12): 5887-5911
- Smooth muscle protein 22-alpha mediated patchy deletion of {Bmpr1a} impairs cardiac contractility but protects against pulmonary vascular remodeling. Circ Res. 2008; (3): 380-388
- Inhibition of Tgf beta signaling by endogenous retinoic acid is essential for primary lung bud induction. Development. 2007; (16): 2969-79
- Distinct roles for retinoic acid receptors alpha and beta in early lung morphogenesis. Dev Biol. 2006; (1): 12-24
- COPD: Clinical Manifestations, Diagnosis, and Treatment Baum's Textbook of Pulmonary Diseases (Eds: James D. Crapo, Jeffrey Glassroth, Joel Karlinsky, and Talmadge E. King Jr.). 2004
- Retinoic acid selectively regulates Fgf10 expression and maintains cell identity in the prospective lung field of the developing foregut. Dev Biol. 2004; (2): 402-15
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