title: Autophagy is decreased in mesenteric fat tissue but not in intestinal mucosae of patients with Crohn's disease.
abstract: Crohn's disease (CD) is a chronic intestinal disease with a multifactorial etiology. Recently, a role for mesenteric fat has been proposed in CD pathophysiology, since fat hypertrophy is detected close to the affected intestinal area; however, there are few studies regarding autophagy and the hypertrophied mesenteric tissue in CD. To evaluate autophagy-related proteins in intestinal mucosae and mesenteric fat of patients with CD and controls, patients with ileocecal CD (CD Group) and with non-inflammatory disease (FC Group) selected for surgery were studied. Expression of LC3-II was determined by immunoblotting of protein extracts. In addition, beclin-1, LC3 and Atg16-L1 RNA levels were measured using RT-PCR. The expression of LC3-II was significantly lower in the mesenteric tissue and higher in intestinal mucosae of CD when compared to controls. However, mRNA expression of autophagy-related proteins was similar when comparing the mesenteric fat groups. These findings suggest a defect in autophagy activation in the mesenteric fat tissue of CD individuals, which could be involved in the maintenance of the inflammatory process.
authors.affiliation: Coloproctology Unit, Surgery Department, University of Campinas, Medical School, São Paulo, Brazil. raquelleal@mpc.com.br
authors.forename: Raquel F
authors.initials: RF
authors.lastname: Leal
authors.forename: Cláudio S R
authors.initials: CS
authors.lastname: Coy
authors.forename: Lício A
authors.initials: LA
authors.lastname: Velloso
authors.forename: Sushila
authors.initials: S
authors.lastname: Dalal
authors.forename: Mariana
authors.initials: M
authors.lastname: Portovedo
authors.forename: Viviane S
authors.initials: VS
authors.lastname: Rodrigues
authors.forename: Andressa
authors.initials: A
authors.lastname: Coope
authors.forename: Maria L S
authors.initials: ML
authors.lastname: Ayrizono
authors.forename: João J
authors.initials: JJ
authors.lastname: Fagundes
authors.forename: Marciane
authors.initials: M
authors.lastname: Milanski
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology*; D051017:Apoptosis Regulatory Proteins / Q000096:biosynthesis / Q000235:genetics; D001343:Autophagy / Q000502:physiology*; D000071183:Autophagy-Related Proteins; D000071186:Beclin-1; D001706:Biopsy; D002352:Carrier Proteins / Q000096:biosynthesis / Q000235:genetics; D003424:Crohn Disease / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism / Q000473:pathology*; D008565:Membrane Proteins / Q000096:biosynthesis / Q000235:genetics; D008869:Microtubule-Associated Proteins / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism
chemical_list: C518959:ATG16L1 protein, human; D051017:Apoptosis Regulatory Proteins; D000071183:Autophagy-Related Proteins; C491997:BECN1 protein, human; D000071186:Beclin-1; D002352:Carrier Proteins; C477012:MAP1LC3A protein, human; D008565:Membrane Proteins; D008869:Microtubule-Associated Proteins; D012333:RNA, Messenger