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The biology and pathobiology of the ECL cells.
Yale J Biol Med. 1992 Nov-Dec; 65(6):761-74; discussion 827-9.YJ

Abstract

The enterochromaffin-like (ECL) cells represent the predominant endocrine cell population in the acid-producing part of the stomach of both experimental animals and man. These cells actively produce and store histamine in addition to an anticipated but as yet unidentified peptide hormone and are under the control of gastrin. An acute gastrin stimulus causes exocytosis of the cytoplasmic granules/vesicles (and release of histamine and activation of the histamine-forming enzyme, histidine decarboxylase), while a more sustained gastrin stimulus causes first hypertrophy and then hyperplasia of the ECL cells in the rat (at most, a fivefold increase in the cell number). These effects can be demonstrated following infusion of gastrin or following an increase in the concentration of circulating gastrin of endogenous origin. The growth of the ECL cells reflects an accelerated self-replication rate. As studied in the rat, the self-replication rate is accelerated quite soon after induction of hypergastrinemia (blockade of acid secretion), the rate is maximally elevated within two weeks and then declines to control values at ten and 20 weeks despite the sustained hypergastrinemia. Lifelong hypergastrinemia in rats is associated not only with ECL-cell hyperplasia but also with an increased incidence of ECL-cell carcinoids. Recently, we could show that alpha-fluoromethylhistidine, which is a suicide inhibitor of histidine decarboxylase, effectively depletes the ECL cells of histamine and that the histamine-depleted ECL cells respond to gastrin with hyperplasia in a manner identical to normal ECL cells. Other factors beside gastrin seem to participate in the control of ECL-cell function and proliferation. Although exogenous somatostatin is known to suppress the activity of the ECL cells, we have failed to obtain evidence that the somatostatin cells in the oxyntic mucosa play a role in the physiological control of the ECL cells. The vagus, however, is important for the ability of the ECL cells to respond to gastrin. This conclusion is based on the observation that vagal denervation suppresses the hyperplastic response of the ECL cells to gastrin. Porta-cava shunting, on the other hand, greatly enhances the responsiveness of the ECL cells to gastrin. The mechanism behind this effect is unknown.

Authors+Show Affiliations

Department of Pharmacology, University of Lund, Sweden.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

1341077

Citation

Håkanson, R, et al. "The Biology and Pathobiology of the ECL Cells." The Yale Journal of Biology and Medicine, vol. 65, no. 6, 1992, pp. 761-74; discussion 827-9.
Håkanson R, Tielemans Y, Chen D, et al. The biology and pathobiology of the ECL cells. Yale J Biol Med. 1992;65(6):761-74; discussion 827-9.
Håkanson, R., Tielemans, Y., Chen, D., Andersson, K., Ryberg, B., Mattsson, H., & Sundler, F. (1992). The biology and pathobiology of the ECL cells. The Yale Journal of Biology and Medicine, 65(6), 761-74; discussion 827-9.
Håkanson R, et al. The Biology and Pathobiology of the ECL Cells. Yale J Biol Med. 1992 Nov-Dec;65(6):761-74; discussion 827-9. PubMed PMID: 1341077.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The biology and pathobiology of the ECL cells. AU - Håkanson,R, AU - Tielemans,Y, AU - Chen,D, AU - Andersson,K, AU - Ryberg,B, AU - Mattsson,H, AU - Sundler,F, PY - 1992/11/1/pubmed PY - 1992/11/1/medline PY - 1992/11/1/entrez SP - 761-74; discussion 827-9 JF - The Yale journal of biology and medicine JO - Yale J Biol Med VL - 65 IS - 6 N2 - The enterochromaffin-like (ECL) cells represent the predominant endocrine cell population in the acid-producing part of the stomach of both experimental animals and man. These cells actively produce and store histamine in addition to an anticipated but as yet unidentified peptide hormone and are under the control of gastrin. An acute gastrin stimulus causes exocytosis of the cytoplasmic granules/vesicles (and release of histamine and activation of the histamine-forming enzyme, histidine decarboxylase), while a more sustained gastrin stimulus causes first hypertrophy and then hyperplasia of the ECL cells in the rat (at most, a fivefold increase in the cell number). These effects can be demonstrated following infusion of gastrin or following an increase in the concentration of circulating gastrin of endogenous origin. The growth of the ECL cells reflects an accelerated self-replication rate. As studied in the rat, the self-replication rate is accelerated quite soon after induction of hypergastrinemia (blockade of acid secretion), the rate is maximally elevated within two weeks and then declines to control values at ten and 20 weeks despite the sustained hypergastrinemia. Lifelong hypergastrinemia in rats is associated not only with ECL-cell hyperplasia but also with an increased incidence of ECL-cell carcinoids. Recently, we could show that alpha-fluoromethylhistidine, which is a suicide inhibitor of histidine decarboxylase, effectively depletes the ECL cells of histamine and that the histamine-depleted ECL cells respond to gastrin with hyperplasia in a manner identical to normal ECL cells. Other factors beside gastrin seem to participate in the control of ECL-cell function and proliferation. Although exogenous somatostatin is known to suppress the activity of the ECL cells, we have failed to obtain evidence that the somatostatin cells in the oxyntic mucosa play a role in the physiological control of the ECL cells. The vagus, however, is important for the ability of the ECL cells to respond to gastrin. This conclusion is based on the observation that vagal denervation suppresses the hyperplastic response of the ECL cells to gastrin. Porta-cava shunting, on the other hand, greatly enhances the responsiveness of the ECL cells to gastrin. The mechanism behind this effect is unknown. SN - 0044-0086 UR - https://www.unboundmedicine.com/medline/citation/1341077/The_biology_and_pathobiology_of_the_ECL_cells_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/1341077/ DB - PRIME DP - Unbound Medicine ER -