Testis and thyroid were also the tissues with the highest expression level of human IRIP, according to the SymAtlas database. We identified the IRIP gene as an I/R-inducible gene in a differential display analysis. Therefore, we examined the expression of IRIP mRNA in mouse kidney at different time points after I/R. In normal kidney, IRIP was expressed at a basal level and it was activated 1.7-, 4.2-, and 5.1-fold after ischemia and at 6 and 24 h of reperfusion, respectively (Fig. Endotoxemia can induce multiple organ ischemia due to microvascular constriction (9). We decided to characterize expression of IRIP in the mouse model of LPS-induced endotoxemia. After LPS administration (16 mg/kg of body weight), the IRIP mRNA level significantly increased in all tested or- gans, such as the liver, lungs, and spleen (Fig. Sustained activation was observed in the liver and lungs up to 18 h and in the spleen up to 8 h. At this moment, the molecular mechanism of IRIP activation in I/R and endotoxemia remains unknown. IRIP was also expressed in mouse fibroblasts (NIH 3T3), prox- imal tubular and mesangial cells, brain cortical neurons (data not shown), and human HeLa and Wish cells. Interestingly, two IRIP transcripts were observed in human cells, with apparent sizes of 1.9 and 1.2 kb, respectively (Fig. Both hIRIP transcripts were cloned and se- quenced. They have identical 5 Ј -end sequences, the same open reading frame, and encode the same protein. The longer transcript contain an additional ϳ 600 bp in the 3 Ј -untranslated region (Fig. Further examination of hIRIP sequence re- vealed two potential polyadenylation signal sites that correspond to the two transcripts, suggesting that they could be the product of alternative polyadenylation (2).
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