THE BIOLOGY AND PHYSIOLOGY OF THE ECL CELL

Citation
R. Hakanson et al., THE BIOLOGY AND PHYSIOLOGY OF THE ECL CELL, The Yale journal of biology & medicine, 67(3-4), 1994, pp. 123-134
Citations number
50
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
00440086
Volume
67
Issue
3-4
Year of publication
1994
Pages
123 - 134
Database
ISI
SICI code
0044-0086(1994)67:3-4<123:TBAPOT>2.0.ZU;2-6
Abstract
The enterochromaffin-like (ECL) cells, which are the predominant endoc rine cell type in the acid-producing part of the vertebrate stomach, a re characterized by numerous, electron-lucent vesicles and few electro n-dense granules in the cytoplasm. The biological and physiological si gnificance of the ECL cells remains poorly understood. They produce an d store histamine and pancreastatin and are thought to produce an as y et unidentified peptide hormone. The most important clue to their func tion is their willingness to respond to changes in circulating gastrin . The present review presents current knowledge of the biology and phy siology of the rat stomach ECL cells. Examination of serially sectione d ECL cells has revealed that the cytoplasmic vesicles almost invariab ly contain an electron-dense core, suggesting that perhaps the distinc tion between granules and vesicles is artificial. We propose a life cy cle of the secretory organelles in the ECL cells with a progressive de velopment from granules to vesicles. The results showed that the gastr in-evoked release of histamine and pancreastatin was accompanied by lo ss of vesicles, and that synthesis of histamine and pancreastatin was accelerated by sustained infusion of gastrin, a treatment that was ass ociated with renewal of vesicles. The events described are instrumenta l in bringing about a change in the ''steady state'' or ''equilibrium' ' of the ECL cells, from a non-stimulated, resting state to a gastrin- stimulated, active state. This change is attained within six to eight hr. The next ''steady state'' change is that from ''normal-sized'' but active ECL cells to ''hypertrophic'' ECL cells. The increase in cell size is complete after about one week. The gastrin-evoked increase in the ECL cell self-replication rate is maximal after about 10 days, aft er which time there is a gradual return back to pre-stimulation values . The ECL cell density increases fairly slowly and does not reach maxi mum (four-fold increase) until after 20 weeks of hypergastrinemia. The activity of the histamine-forming enzyme, histidine decarboxylase, is elevated by gastrin and remains elevated for as long as the gastrin s timulus is maintained (the longest time studied was 20 weeks). The phy siological significance of the ECL cells is probably related to their capacity to produce and store histamine and an as yet unidentified pep tide hormone. The ECL cells are thought to be the source of histamine necessary for the gastrin-evoked acid response. In addition, prelimina ry evidence suggests that the ECL cells and the anticipated ECL cell h ormone play a role in bone formation.