Physiology of gastric enterochromaffin-like cells.
Enterochromaffin-like (ECL) cells are neuroendocrine cells in the gastric mucosa that control acid secretion by releasing histamine as a paracrine stimulant. The antral hormone gastrin and the neural messenger pituitary adenylyl cyclase- activating peptide (PACAP) potently stimulate histamine synthesis, storage, and secretion by ECL cells. Histamine is stored in secretory vesicles via V-type ATPases and vesicular monoamine transporters of subtype 2 (VMAT-2). Plasmalemmal calcium entry occurs via L-type calcium channels upon stimulation with secretagogues. K(+) and Cl(-) channels maintain the membrane potential. Calcium-triggered exocytosis of histamine is mediated by interacting SNARE proteins, especially by synaptobrevin and SNAP-25. Dynamins and amphiphysins appear to play a key role in endocytosis. ECL cells are under transcriptional control of various hormones. Gastrin stimulates transcriptional activity of the histidine decarboxylase ( HDC), VMAT-2, and chromogranin A promoter by activation of Sp1 elements and CREB. During chronic Helicobacter pylori infection, pro-inflammatory cytokines are released that can also affect ECL cells, thus impairing their secretory function and viability, which can predispose to hypochlorhydria and gastric carcinogenesis.[1]References
- Physiology of gastric enterochromaffin-like cells. Prinz, C., Zanner, R., Gratzl, M. Annu. Rev. Physiol. (2003) [Pubmed]
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