- 作者：Mohammad S. Rahnama’ ; i ; Sajjad_r@yahoo.com ; Bart T. Biallosterski ; Stefan G.G. de Wachter ; Philip E.V. Van Kerrebroeck ; Gommert A. van Koeveringe
- 关键词：PG ; prostaglandin ; PGE2 ; prostaglandin E2 ; EP1 ; prostaglandin E receptor type 1 ; EP2 ; prostaglandin E receptor type 2 ; COX I ; cyclo-oxygenase type 1 ; DO ; detrusor overactivity ; OAB ; overactive bladder syndrome ; ICs ; interstitial cells ; IM-ICs ; intramuscle
- 刊名：Prostaglandins and Other Lipid Mediators
- 出版年：2012
- 出版时间：December, 2012
- 年：2012
- 卷：99
- 期：3-4
- 页码：107-115
- 全文大小：2607 K
Objective
To explore the distribution of prostaglandin E receptor type 2 (EP2) in the bladder muscle layers and its spatial relationship to cyclo-oxygenase type 1 (COX I).Materials and methods
Twelve male guinea pigs were killed by cervical dislocation, the bladders removed and fixed in 4 % paraformaldehyde in PBS. Frozen sections of 10 ¦Ìm were cut and stained with antibodies to EP2, COX I and vimentin.
Results
EP2 receptor immunoreactivity is located on the smooth muscle cells as well as on vimentin positive surface muscle and intramuscular interstitial cells. EP2 expression on interstitial cells is highly localized. Discrete regions of intense staining were observed on the interstitial cell processes. COX I is expressed in the muscle interstitial cells and was found to be located on discrete regions of the cell and cell processes. Double staining with EP2 and COX I suggests that the regions of a cell expressing EP2 are different from those expressing COX I.
Conclusions
The presence of COX I, prostaglandin E receptor type 2 (EP2) immune-reactivity in the network of interstitial cells suggests a role of this network in the propagation of signals. Due to a cAMP coupling of the EP2 receptor in many other tissues and a lower dissociation constant of EP2, it is suggested that a rise in PG levels may gradually push the balance from a relaxant EP2 effect towards a contractile effect. Hence, PG could have a modulatory role on the non-voiding bladder contractions by changing the threshold level for excitability of the interstitial cell network.