Abstract
Introduction:
X-irradiation induced the cell death by apoptosis in mucosal epithelial cells, and caused the impairment of physiological varrier against many antigens in gut lumen. Angiopoietin family is well known as a vasculogenic factor that signals through the Tie-2 receptor tyrosine kinase. Some groups reported that Angiopoietin (Ang)-1 prevented apoptosis induced by serum deprivation in endothelial cells of vasculature, through the regulation of signaling pathways.
Aim & Methods:
To elucidate the effect of Angiopoietin family in the normal intestinal epithelial cells, IEC-18 cell was treated with recombinant human Ang-1 (rhAng-1) or rhAng-2 followed by X-ray irradiation of 10Gy and then examined for the regulation of viability by the phosphatidylinositol 3-kinase (PI3K) and/or mitogen activated protein kinase (MAPK) pathway. Cell viability was counted by trypan blue staining and the TUNEL assay.
Results:
X-irradiation induced the cell death of IEC-18. When compared with non-rhAng-1 treated cells, the viability of the X-irradiated IEC-18 cells was up-regulated by rhAng-1 treatment and also resulted in the induction of phosphorylation of S6 ribosomal protein that represented the activity of PI3K pathway. However, p90 RSK and p38MAPK pathways were not up-regulated by rhAng-1 treatment. The activation of caspase-3 induced by X-irradiation was decreased with treatment of rhAng-1. However, the treatment of rhAng-2 did not show any protective effect on the cell death of IEC-18 with X-irradiation. Any activation of PI3K, p90RSK and p38MAPK pathways were not regulated by rhAng-2 in IEC-18 cell.
Conclusions:
These results suggested that Ang-1 has the possibility of protective effect in the intestinal disorder induced by X-irradiation.
