Tag: Annie Zemper

Characterization of Lrig1 Positive Stem Cells During Colitis Recovery

Presenter(s): Nicholas Jahahn − General Science

Faculty Mentor(s): Annie Zemper

Oral Session 4S

Research Area: Natural/Physical Science

Funding: National Institute of Diabetes and Digestive and Kidney Diseases, OURS program at the university of Oregon through NIH award

The intestine is a highly regenerative organ in humans and mice. Within the epithelium, structures called crypts contain epithelial stem cells that repopulate the intestinal mucosa. Lrig1 is an ErbB negative regulator that marks a population of stem cells in the base of the intestinal crypts. To study intestinal epithelium in a disease state, Dextran sodium sulfate (DSS) was used to induce ulcerative colitis in mice, characterized by inflammation of the distal colon epithelia. Here we examined the role of Lrig1 positive stem cells in colitis recovery. To accomplish this, we utilized transgenic mice that expressed Cre recombinase protein from the Lrig1 promoter and expressed YFP protein from the ROSA locus. Lineage tracing was carried out to observe what stem cells give rise to when the mouse is treated with DSS. Immunofluorescent analysis was conducted to visualize the localization of Lrig1 positive stem cells and their progeny in the wound healing process for comparison between homeostasis and different durations of recovery. It was observed that at both 36 and 48 hours after a weeklong assault of DSS there was a greater percentage of lineage traced cells found higher in the crypt compared to homeostatic conditions. We further observed that proliferation of the lineage traced cells followed the same trend. These results indicate that Lrig1 stem cells do actively participate in the recovery process. Where exactly the Lrig1 stem cells that participate in recovery originate from will be addressed with further lineage tracing closer to the time of cessation of DSS.

Exploring the Role of Lrig3 In the Colon

Presenter(s): Ryan Sayegh

Faculty Mentor(s): Annie Zemper & Janelle Stevenson

Poster 9

Session: Sciences

The colon is a vital organ for digestion. Its inner epithelial lining has tubular invaginations known as colonic crypts. These crypts contribute to a dynamic system containing stem cells necessary for colonic repair and maintenance (Barker et al. 2014). Disruption of the colonic crypt system is a symptom of diseases like Irritable Bowel Disease, colitis, and colorectal cancer. The protein EGFR plays an important role in the cell proliferation necessary for maintaining homeostasis within the colon. Leucine-rich repeats and immunoglobulin like domains 1 (Lrig1) is a protein that plays an antagonizing role to Egfr (Wang et al. 2013). LRIG3, a homolog of LRIG1 was shown to positively regulate EGFR in a cell culture model (Rafidi et al. 2013). However, its role in the colon remains unknown. I hypothesize that mice lacking Lrig3 (Lrig3-/-) will have smaller epithelial tissue areas with lower expression of Egfr. I used immunofluorescence to analyze the expression of Egfr in the absence of Lrig3 and found no difference compared to control mice. I then analyzed colonic epithelial area using Hematoxylin and Eosin staining and found that Lrig3- /- mice had a larger area of epithelial tissue when compared to control mice. These data show that Lrig3 may be playing a different role in the Egfr pathway than what other models would suggest.