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.MATERIALS AND 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.CONCLUSION: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.

RING finger protein 10 attenuates vascular restenosis by inhibiting vascular smooth muscle cell hyperproliferation in vivo and vitro

“…In addition, AP‐1, a key transcription factor, is predicted to have binding sites to RING finger family members and function in cell proliferation . Due to the synergistic effects of AP‐1 on various physiological activities, its inhibitors are always applied to many cardiovascular diseases . Furthermore, the attenuation of AP‐1 has been confirmed to limit vascular restenosis after PCI .…”

The protective mechanism of Nigella sativa against diethylnitrosamine‐induced hepatocellular carcinoma through its antioxidant effect and EGFR/ERK1/2 signaling

“…The PCR program started with 30 min at 45°C (reverse transcription reaction), then 5 min at 95°C (inactivation of RTase), 1 min for an extension at 72°C and 5 min final extension at 72°C for each primer. The specific primers sequences and size are listed in Table . The PCR products were resolved by electrophoresis through an agarose gel (1.5%) and stained with ethidium bromide .…”

“…The specific primers sequences and size are listed in Table 2. 22,[47][48][49] The PCR products were resolved by electrophoresis through an agarose gel (1.5%) and stained with ethidium bromide. 50 The band intensity was quantified using image-analyzing system (UVIBAND MAX software program).…”

Inhibitory effect of Bailing capsule on hypoxia-induced proliferation of rat pulmonary arterial smooth muscle cells

“…The cellular genes c-fos and c-jun dimerize to form the activator protein-1 transcription factor complex, which upregulates transcription of a diverse range of genes. 25 These genes are involved in proliferation, differentiation, and in a series of pathophysiological processes. 26 Furthermore, c-jun and c-fos are both induced under hypoxic conditions and may increase proliferation rate of PASMCs.…”