Selective stimulation of the PGE2 signal through EP2 receptors by a specific agonist promoted regeneration of cartilage tissues with a physiological osteochondral boundary, suggesting the potential usefulness of this small molecule for the treatment of injured articular cartilages.

Although the level of prostaglandin (PG) D 2 in cerebrospinal fluid (CSF) affects the action of D-type prostanoid receptors that promote physiological sleep, the regulatory system of PGD 2 clearance from the CSF is not fully understood. The purpose of this study was to investigate PGD 2 elimination from the CSF via the blood-CSF barrier (BCSFB). The in vivo PGD 2 elimination clearance from the CSF was 16-fold greater than that of inulin, which is considered to reflect CSF bulk flow. This process was inhibited by the simultaneous injection of unlabeled PGD 2 . The characteristics of PGD 2 uptake by isolated choroid plexus were, at least partially, consistent with those of PG transporter (PGT) and organic anion transporter 3 (OAT3). Studies using an oocyte expression system showed that PGT and OAT3 were able to mediate PGD 2 transport with a Michaelis-Menten constant of 1.07 and 7.32 M, respectively. Reverse transcription-polymerase chain reaction and immunohistochemical analyses revealed that PGT was localized on the brush-border membrane of the choroid plexus epithelial cells. These findings indicate that the system regulating the PGD 2 level in the CSF involves PGT-and OAT3-mediated PGD 2 uptake by the choroid plexus epithelial cells, acting as a pathway for PGD 2 clearance from the CSF via the BCSFB.

No abstract