title: Immediate expression of c-fos and c-jun mRNA in a model of intestinal autotransplantation and ischemia-reperfusion in situ.
abstract: OBJECTIVE
  Intestinal ischemia-reperfusion injury occurs in several clinical conditions and after intestinal transplantation. The aim of the present study was to investigate the phenomena of apoptosis and cell proliferation in a previously described intestinal ischemia-reperfusion injury autograft model using immunohistochemical markers. The molecular mechanisms involved in ischemia-reperfusion injury repair were also investigated by measuring the expression of the early activation genes c-fos and c-jun, which induce apoptosis and cell proliferation.
  
  
  METHODS
  Thirty adult male Wistar rats were subjected to surgery for a previously described ischemia-reperfusion model that preserved the small intestine, the cecum and the ascending colon. Following reperfusion, the cecum was harvested at different time points as a representative segment of the intestine. The rats were allocated to the following four subgroups according to the reperfusion time: subgroup 1: 5 min; subgroup 2: 15 min; subgroup 3: 30 min; and subgroup 4: 60 min. A control group of cecum samples was also collected. The expression of c-fos, c-jun and immunohistochemical markers of cell proliferation and apoptosis (Ki67 and TUNEL, respectively) was studied.
  
  
  RESULTS
  The expression of both c-fos and c-jun in the cecum was increased beginning at 5 min after ischemia-reperfusion compared with the control. The expression of c-fos began to increase at 5 min, peaked at 30 min, and exhibited a declining tendency at 60 min after reperfusion. A progressive increase in c-jun expression was observed. Immunohistochemical analyses confirmed these observations.
  
  
  CONCLUSIONS
  The early activation of the c-fos and c-jun genes occurred after intestinal ischemia-reperfusion injury, and these genes can act together to trigger cell proliferation and apoptosis.
authors.forename: Maria Mercês
authors.initials: MM
authors.lastname: Santos
authors.forename: Ana Cristina Aoun
authors.initials: AC
authors.lastname: Tannuri
authors.forename: Maria Cecilia Mendonça
authors.initials: MC
authors.lastname: Coelho
authors.forename: Josiane de Oliveira
authors.initials: Jde O
authors.lastname: Gonçalves
authors.forename: Suellen
authors.initials: S
authors.lastname: Serafini
authors.forename: Luiz Fernando Ferraz da
authors.initials: LF
authors.lastname: Silva
authors.forename: Uenis
authors.initials: U
authors.lastname: Tannuri
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics; D049109:Cell Proliferation / Q000235:genetics; D050377:Cold Ischemia / Q000379:methods; D015870:Gene Expression; D017781:Genes, Immediate-Early; D016762:Genes, fos; D016758:Genes, jun; D007150:Immunohistochemistry / Q000379:methods; D020287:In Situ Nick-End Labeling; D007421:Intestine, Small / Q000098:blood supply* / Q000378:metabolism / Q000637:transplantation; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D023421:Models, Animal; D012333:RNA, Messenger / Q000378:metabolism*; D017208:Rats, Wistar; D060888:Real-Time Polymerase Chain Reaction / Q000379:methods; D015427:Reperfusion Injury / Q000235:genetics / Q000378:metabolism*
chemical_list: D019394:Ki-67 Antigen; D012333:RNA, Messenger