Robert Dettman

  • 1700 Citations
1990 …2019

Research output per year

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Personal profile

Research Interests

My interest is in cell fate decisions that lead either to normal development or pathology. In many cases, epithelial cells are induced to undergo cell-shape and migratory changes that allow them to become mesenchymal fibroblasts. This is a process called epithelial-mesenchymal transition or EMT. Fibroblasts then differentiate into new cell types or, in the case of fibrotic disease, abnormal myofibroblasts. In the bladder, outlet obstruction leads to permanent changes to the bladder wall resulting in either a small, high resistance bladder or a very large, atonic bladder. In either case, this leads to difficulties in emptying the bladder and this causes retrograde pressure on the ureters and kidney injury. While clinically this problem is well understood, little is known about the cellular changes that affect the bladder wall. We are using Cre-loxP cell labeling techniques in combination with a bladder outlet obstruction model in mice. Current projects involve the use of the "Confetti" reporter to label small clones of cells in the adult bladder prior to injury. Inducible Cre expression in the urothelium, stroma and serosa will activate the color in these cells and bladders will be injured. We will then be able to determine which cells contribute myofibroblasts to the bladder wall and if this involves EMT. A second interest is in bladder regeneration. It is well reported that the bladder can re-grow after resection. It is also known that when acellular, extracellular matrix patches are used to replace resected bladders that endogenous cells migrate and repopulate the acellular patch (AKA augment). We have found that re-growth of the bladder after resection involves partial regeneration of the bladder in association with fibrotic changes to the bladder wall throughout the entire bladder. Future studies will be to study cell fates during regeneration (using Cre labeling) as well as drugs that could potentially improve the way in which the bladder regenerates.

Training Experience

1999Postdoctoral Fellowship, University of California, San Francisco

Education/Academic qualification

PhD, Indiana University Bloomington

… → 1994

Research interests

  • Bladder and Urinary Tract
  • Cell Adhesion Mechanisms
  • Cell Biology
  • Connective Tissue Biology
  • Developmental Biology
  • Developmental Genetics
  • Fibrosis
  • Stem Cells

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Research Output

  • 1700 Citations
  • 28 Article
  • 2 Editorial
  • 1 Short survey

Stem cell antigen/Ly6a protects against bladder fibrosis in mice

Tassone, N. M., Li, B., Patel, M. S., Devine, M. Y., Firmiss, P. R., Gould, A. D., Kochan, K. S., Stubbee, R. A., Bowen, D. K., Dettman, R. W. & Gong, E. M., 2019, In : American Journal of Physiology - Renal Physiology. 317, 6, p. F1503-F1512

Research output: Contribution to journalArticle

  • 1 Scopus citations

    The Homeodomain Transcription Factor NKX3.1 Modulates Bladder Outlet Obstruction Induced Fibrosis in Mice

    Patel, M. S., Bowen, D. K., Tassone, N. M., Gould, A. D., Kochan, K. S., Firmiss, P. R., Kukulka, N. A., Devine, M. Y., Li, B., Gong, E. M. & Dettman, R. W., Nov 12 2019, In : Frontiers in Pediatrics. 7, 446.

    Research output: Contribution to journalArticle

    Open Access
  • 1 Scopus citations

    Compensatory regrowth of the mouse bladder after partial cystectomy

    Delos Santos, G. B., Devine, M. Y., Wetterlin, J., Firmiss, P. R., Kukulka, N. A., Bowen, D. K., Gong, E. M. & Dettman, R. W., Nov 2018, In : PloS one. 13, 11, e0206436.

    Research output: Contribution to journalArticle

  • 1 Scopus citations

    Intrauterine growth restriction and hyperoxia as a cause of white matter injury

    Chang, J. L., Bashir, M., Santiago, C., Farrow, K., Fung, C., Brown, A. S., Dettman, R. W. & Dizon, M. L. V., Dec 1 2018, In : Developmental Neuroscience. 40, 4, p. 344-357 14 p.

    Research output: Contribution to journalArticle

  • 1 Scopus citations