ABSTRACT
Plasma pH can be altered during pregnancy and at labor. Membrane excitability of smooth muscle including uterine muscle is suppressed by the activation of K(+) channels. Because contractility of uterine muscle is regulated by extracellular pH and humoral factors, K(+) conductance could be connected to factors regulating uterine contractility during pregnancy. Here, we showed that TASK-2 inhibitors such as quinidine, lidocaine, and extracellular acidosis produced contraction in uterine circular muscle of mouse. Furthermore, contractility was significantly increased in pregnant uterine circular muscle than that of non-pregnant muscle. These patterns were not changed even in the presence of tetraetylammonium (TEA) and 4-aminopyridine (4-AP). Finally, TASK-2 inhibitors induced strong myometrial contraction even in the presence of L-methionine, a known inhibitor of stretchactivated channels in myometrium. When compared to non-pregnant myometrium, pregnant myometrium showed increased immunohistochemical expression of TASK-2. Therefore, TASK-2, seems to play a key role during regulation of myometrial contractility in the pregnancy and provides new insight into preventing preterm delivery.
ABSTRACT
This study was executed to prove the existence of c-Kit-positive interstitial cells of Cajal (ICC)-like cells [c-Kit (+) ICC-like cells] and their possible role associated with gastric inflammation and/or carcinogenesis in human gastric mucosa. c-Kit (+) ICC-like cells were observed throughout all the layers of the gastric fundus along the greater curvature. Dense fusiform cell bodies with many processes were found in each layer. We also studied the c-Kit-positive immunoreactivity distribution pattern in the mucosa. c-Kit (+) cells were found mainly around the epithelial repair zone of the normal gastric fundus/corpus and of the fundus/corpus with non-metaplastic chronic gastritis. Notably, they were found attached to the epithelia of the repair zone in non-metaplastic chronic gastritis. In chronic gastritis with intestinal metaplasia, they were found scattered everywhere in the stroma of the gastric mucosa and did not attach to the metaplastic epithelium. We found c-Kit (+) ICC-like cells in human mucosa. They were present mainly in the stroma around the repair zone of the glands in chronic gastritis as well as in normal mucosa, whereas they seemed to redistribute over the whole mucosa in gastritis with intestinal metaplasia. These cells around the repair zone were found to be tightly attached to epithelial cells, but not to metaplastic epithelial cells. Thus, c-Kit (+) ICC-like cells appear to have a role in the epithelial recovery process and may be associated with carcinogenesis of human gastric mucosa.
