Study of the two UDPglucose-Glycoprotein glucosyltransferase (UGGT) homologues in a mouse model of intestinal inflammation

ANA EMILIA BOTTERO; MARÍA ROCÍO RIAL HAWILA; GABRIELA ACOSTA ; MARÍA ESTELA ROUX; OLGA A CASTRO; SILVIA MIRANDA

Buenos Aires

Congreso; Primer Congreso Internacional LASID-SAI-FAIC; 2015

LASID-SAI-FAIC

Background: Intestinal epithelial cells (IEC) areparticularly susceptible to endoplasmic reticulum stress. UPR (unfolded protein response) is required tomaintain IEC homeostasis and its impairment can lead to inflammation asobserved in Crohn´s disease. UGGT is the key component of the quality controlmechanism of glycoprotein folding. We have previously described a second isoformin mouse and C. elegans.  In this study, we explored UGGTs expression inmouse small intestine and their modulation by accoustic stimuli (AS), a modelof Crohn´s disease.Methods: CBA/Jmice were exposed to 24h AS (300Hz-70dB) and randomized (n=5). Mice werekilled: 1) after AS; 2) three weeks after AS; 3) mice were submitted to AS oncea week during a month and then were killed. Control groups did not receive AS. UGGT1/UGGT2 expression was analyzed intissue sections by immunohistochemical analysis. To this aim, antiserum anti-UGGT2was raised in rabbits employing a multiantigenic peptide synthesized with a sequenceof UGGT2 (NP_001074721.2) not present in UGGT1 (NP_942602.2). The specificity wasconfirmed by western blot.Results: UGGTsare moderately expressed in normal conditions. After one (1) or various AS (3),UGGT1/UGGT2 expression increased proportionally to inflammation (for both: group3>1, p