PARENT SESSION
GENE REGULATION AND FUNCTION IN THE REPRODUCTIVE AXIS
Kent
7:30 AM-10:00 AM

(382) DIFFERENTIAL ROLE OF TNFRII IN AN ANIMAL MODEL OF INTESTINAL ENDOMETRIOSIS.

Rojas-Cartagena, Carmencita¹, Appleyard, Caroline¹, Santiago, Olga¹, Santiago, Cariluz¹, Resto, Karina¹, Flores, Idhaliz¹, ¹ Ponce School of Medicine, Ponce, PR

ABSTRACT- Symptoms of intestinal endometriosis often mimic other gastrointestinal disorders, leading to misdiagnosis and improper therapy. Although TNF- appears to play a role in both diseases its contribution to each remains unclear. OBJECTIVE: To compare the expression of TNF- and TNFRII in an animal model of intestinal endometriosis. METHODS: Sexually mature female Sprague-Dawley rats were used for the model. Intestinal endometriosis was surgically induced by suturing uterine horn implants next to the mesentery of the small intestine (control: sutures with no implants) for 60 days. Peritoneal fluid and tissues were collected from all animals, implants were classified in grades of growth and the colons were examined for macroscopic damage. Following RNA isolation, relative gene specific RT-PCR was performed to analyze TNF- and TNFRII expression relative to the internal control (IC; 18s rRNA). Band intensities were quantified by densitometry and normalized to IC. RESULTS: TNF- expression was increased in the small intestine of the experimental rats compared to controls (2.0-fold higher). The expression of TNFRII in the small intestine of the experimental rats was lower than in controls (4.0-fold lower). These animals had significantly more white blood cells (wbc) in peritoneal fluid (p<0.05) and significantly higher colonic damage (p<0.05) than their controls. CONCLUSIONS: The increased expression of TNF- in intestinal endometriosis may be responsible for promoting the inflammation in the intestine, and increasing the number of wbc in the peritoneal fluid. The decreased expression of TNFRII could be due to the capacity of TNF- to downregulate its own receptor when the levels of TNF- are high, possibly as a mechanism for maintenance of the balance between cell death and proliferation. Supported in part by MBRS & RCMI.

KEY WORDS: TNF-alpha, TNFR2, intestinal endometriosis