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Decay-Accelerating Factor in Guinea Pig Stomachs Following Ischemia Reperfusion Stress¹

Tadayuki Oshima^*,, Noriko Okada^*, Takashi Joh, Makoto Sasaki, Toyohiro Tada, Noriyuki Matsukawa^,¶, Tomoyuki Nomura, Hirotaka Ohara, Makoto Itoh and Hidechika Okada^2,*

^* Department of Molecular Biology, First Department of Internal Medicine, Department of Pathology, and Second Department of Internal Medicine, Nagoya City University School of Medicine, Nagoya, Japan; and ^¶ Choju Medical Institute, Fukushimura Hospital, Toyohashi, Japan

A complement regulatory protein, decay-accelerating factor (DAF, CD55), is known to protect host tissues from autologous complement activation. DAF is present on the apical side of human gastric epithelial cells, and its expression increases during gastritis. To develop an animal model for analysis of DAF expression on gastric cells, a mAb to guinea pig DAF was successfully used. Although DAF expression in the mucosal epithelium of the stomach is weak, as judged by immunohistochemical staining with the mAb, it was temporarily up-regulated at 12 and 24 h, and at 3 days after ischemia reperfusion (I/R) (p < 0.05). The DAF mRNA level in gastric tissues was determined by Northern blot analysis and found to be highest at 6 h after I/R, returning to the baseline at 24 h. Strong DAF mRNA expression was observed in the cytoplasm of cells beneath the eroded tissues 6 h after I/R. In guinea pigs, alternative splicing of DAF mRNA generates both GPI-anchored types and transmembrane types of DAF. RT-PCR analysis revealed that mRNAs of the transmembrane types had become significantly dominant by 6 h after I/R, whereas levels for the GPI-anchored types remained unchanged. In guinea pigs depleted of complement by cobra venom factor treatment, the area of erosion and the up-regulation of DAF expression in gastric epithelial cells after I/R were significantly limited compared with the normocomplementemic group, indicating that DAF may be up-regulated by an inflammatory stress.

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