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Marshall H. Montrose, PhD
Professor and Dean of the Graduate School

Our laboratory is interested in the cellular and sub-cellular physiology of epithelial cells lining the gastrointestinal tract. In all our projects we explore the role of specific proteins through the use of normal and mutant mice as well as tissue culture models. Our favorite tool is high-resolution (confocal and two-photon) light microscopy, to help us explore and measure events in living cells and tissues.

In the stomach, we are exploring the reason that the stomach does not digest itself despite having a caustic environment imposed on the epithelial cells lining the stomach. Part of the gastric defenses include pH microdomains near the tissue surface, which we detect with confocal microscopy in vivo. The epithelial cells are responsible for both acid and alkali secretion, and here we have explored how changes in the luminal pH of the stomach regulate the dramatic transition from net-acid to net-alkali secretion, and its impact on gastric defense. We are also using the two-photon microscope to cause microscopic lesions in the stomach (damaging 2 to 5 cells) and following in real time the process of expanding damage and repair. Using this model, we have learned that the gastric pathogen Helicobacter pylori rapidly homes in on sites of damage and delays repair within minutes. We have also discovered that the mobilization of both intracellular and extracellular calcium ions is a necessary signal to drive efficient and rapid repair. Curiously, that repair pathway seems to require the activity of both secreted trefoil factor peptides (notably TFF2) and a Na/H exchange transport protein (NHE2) that resides in the apical membrane of the gastric surface epithelium.

Recently we have been excited by the capability to study these processes and pathways using gastric organoids, hollow spheroids of cells derived from tissue stem cells in the stomach. This model provides us a route to rapidly analyze signaling pathways using cells with the same genetic background as our normal and mutant mouse models.

Selected Publications:
  • Eitaro Aihara, Andrea L. Matthis, Rebekah A. Karns, Kristen A. Engevik, Peihua Jiang, Jiang Wang, Bruce R. Yacyshyn, and Marshall H. Montrose (2016) Epithelial regeneration after gastric ulceration causes prolonged cell-type alterations. Cell. Mol. Gastroenterol. Hepatol. 2: 625-647.
  • Andrea L. Matthis, Bin Zhang, Lee A. Denson, Bruce R. Yacyshyn, Eitaro Aihara, and Marshall H. Montrose (2016) Importance of the evaluation of N-acetyltransferase enzyme activity prior to 5-aminosalicylic acid medication for ulcerative colitis. Inflamm. Bowel Dis. 22: 1793-1802.
  • Eitaro Aihara, Chet Closson, Andrea L. Matthis, Michael A. Schumacher, Amy C. Engevik, Yana Zavros, Karen M. Ottemann, and Marshall H. Montrose (2014) Motility and chemotaxis mediate the preferential colonization of gastric injury sites by Helicobacter pylori. PLoS Pathog. 10: e1004275.
  • Eitaro Aihara, Courtney L. Hentz, Abraham M. Korman, Nicholas P. J. Perry, Vikram Prasad, Gary E. Shull, and Marshall H. Montrose (2013) In vivo epithelial wound repair requires mobilization of endogenous intracellular and extracellular calcium. J. Biol. Chem. 288: 33585-33597.
  • Lin Xue, Eitaro Aihara, Timothy C. Wang, and Marshall H. Montrose (2011) Trefoil factor 2 requires Na/H exchanger 2 activity to enhance mouse gastric epithelial repair. J. Biol. Chem. 286: 38375-38382.

Publications, Complete List at PubMed

Postdoctoral positions are currently available in the Montrose laboratory. For information and application details, click here.

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