Abstract
In the present study, we investigated whether prostaglandin E1 (PGE1) could accelerate the disposal of heat-aggregated BSA (a-BSA) in the glomerulus by mesangial cells and/or resident mesangial cells. ICR mice were injected i.v. with 90 mg/100 g B.W. of a-BSA 3 times at 4-hr intervals. Kidneys were isolated at various times after the first injection of a-BSA. The location of a-BSA in the glomerulus was then detected by immunohistochemical staining and immunofluorescence. A-BSA was detected in the mesangium and along capillary walls by both techniques. The amount of glomerular a-BSA increased with time, attaining a peak about 12 to 14 hr after the first administration of a-BSA and then disappeared by 36 hr after. The mice injected with a-BSA 3 times received 150, 200, 300 and 400 μg/mouse of PGE1, s.c., and 200 and 400 μg/mouse of PGE2 or PGF2α, s.c., at 12 hr; and their kidneys were isolated at 16 hr. The mice with 300 and 400 μg/mouse of PGE1 had 34.3% and 37.6% less a-BSA than the control mice, respectively. Additionally, the mice with 400 μg/mouse of PGE2 had 63.2% less a-BSA than the control mice. However, PGF2α failed to reduce glomerular a-BSA to a level less than that of the control. In conclusion, we confirmed that PGE1 accelerates breakup of macromolecules by mesangial cells and/or resident mesangial cells in the glomerulus.
