PGE2 Regulates Pacemaker Currents through EP2-Receptor in Cultured Interstitial Cells of Cajal from Murine Small Intestine

The interstitial cells of Cajal (ICCs) are the pacemaker cells in gastrointestinal tract and generate electrical rhythmicity in gastrointestinal muscles. Therefore, ICC may be modulated by endogenous agents such as neurotransmitter, hormones, and prostaglandins (PGs). In the present study, we investigated the effects of prostaglandins, especially PGE2, on pacemaker currents in cultured ICCs from murine small intestine by using whole-cell patch clamp techniques. ICCs generated spontaneous slow waves under voltage-clamp conditions and showed a mean amplitude of -452+/-39 pA and frequency of 18+/-2 cycles/min (n=6). Treatments of the cells with PGE2 (1muM) decreased both the frequency and amplitude of the pacemaker currents and increased the resting currents in the outward direction. PGE2 had only inhibitory effects on pacemaker currents and this inhibitory effect was dose-dependent. For characterization of specific membrane EP receptor subtypes, involved in the effects of PGE2 on pacemaker currents in ICCs, EP receptor agonists were used: Butaprost (1muM), EP2 receptor agonist, reduced the spontaneous inward current frequency and amplitude in cultured ICCs (n=5). However sulprostone (1muM), a mixed EP1 and EP3 agonist, had no effects on the frequency, amplitude and resting currents of pacemaker currents (n=5). SQ-22536 (an inhibitor of adenylate cyclase; 100muM) and ODQ (an inhibitor of guanylate cyclase; 100muM) had no effects on PGE2 actions of pacemaker currents. These observations indicate that PGE2 alter directly the pacemaker currents in ICCs, and that the PGE2 receptor subtypes involved are the EP2 receptor, independent of cyclic AMP- and GMP-dependent pathway.

A Case with Systemic Lupus Erythematosus Complicated with Multifocal Osteoarticular Tuberculosis / 대한류마티스학회지

Infection is a frequent problem in patients with systemic lupus erythematosus (SLE). Infections contribute greatly to the morbidity of patients and are one of the commonest causes of death. The high frequency and unusual spectrum of infections can be attributed to the multiple disturbances of immune function in SLE in combination with the effects of immunosuppressive therapy. There is increasing evidence to indicate that opportunistic infections including tuberculosis make a large contribution to the infectious mortality in SLE. Tuberculosis is a major cause of morbidity and mortality, particularly in our country where tuberculosis is still endemic. The indolent nature of tuberculous bone and joint disease often leads to delayed or missed diagnosis, sometimes with devastating consequences for the patient. We report a case of multifocal and complicated osteoarticular tuberculosis developing in the spines and knee joint due to delayed diagnosis, with review of literatures.