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PubMed1985

Ultrastructure of midgut endocrine cells in the adult mosquito, Aedes aegypti.

The ultrastructure of endocrine cells in the midgut of the adult mosquito, Aedes aegypti, resembled that of endocrine cells in the vertebrate gastro-intestinal tract. Midgut endocrine cells, positioned basally in the epithelium as single cells, were cone-shaped and smaller than the columnar digestive cells. The most distinctive characteristic of endocrine cells was numerous round secretory granules along the lateral and basal plasma membranes where contents of the granules were released by exocytosis. Secretory granules in each individual cell were exclusively of one type, either solid or 'haloed', and for all cells observed, the range in granule diameter was 60-120 nm. The cytoplasm varied in density from clear to dark. Lamellar bodies were prominent in the apical and lateral cellular regions and did not exhibit acid phosphatase activity. The basal plasma membrane was smooth adjacent to the basal lamina, whereas in digestive cells the membrane formed a labyrinth. Some endocrine cells reached the midgut lumen and were capped by microvilli; a system of vesicles and tubules extended from beneath the microvilli to the cell body. An estimated 500 endocrine cells were distributed in both the thoracic and abdominal regions of the adult midgut. In one midgut, we classified a sample of endocrine cells according to cytoplasmic density and granule type and size; endocrine cells with certain types of granules had specific distributions within the midgut.

Aedes↗

PubMed1982

Acinar-endocrine cell tumor of the pancreas. Report of a pancreatic tumor containing both zymogen and neuroendocrine granules.

A case of pancreatic tumor with features of both an acinar cell and an endocrine cell tumor is presented. The histologic appearance of the tumor by light microscopy was consistent with the appearance of either an islet cell tumor or an acinar cell tumor. Electron microscopy revealed two distinct populations of membrane bound granules within the same tumor cells; namely, a small granule measuring 100-200 nanometers in diameter with a narrow halo separating it from the granule membrane, and a large granule measuring 400-500 nanometers in diameter and having a closely applied membrane. The smaller granules have the characteristic appearance of gastroenteropancreatic (GEP) endocrine-cell granules. The large granules are greater in size than neuroendocrine granules, their morphologic structure is most consistent with that of zymogen granules, and a positive lipase stain supported the presence of zymogen granules within the tumor. The occurrence of both neuroendocrine and zymogen granules within the same cell has been previously described in the "intermediate cell" of the pancreas, but not to our knowledge in a tumor of the pancreas. The finding of both endocrine and exocrine granules within a single cell indicates a histogenetic relationship between the pancreatic endocrine and exocrine cells, and may represent the first reported case of a neoplastic proliferation of intermediate cells.

Adenoma, Islet Cell↗

PubMed2003

Carcinogenesis of gastric endocrine cell carcinoma: analysis of histopathology and p53 gene alteration.

BACKGROUND: Endocrine cell carcinoma of the stomach is characterized by endocrine differentiation and aggressive biological behavior, and is frequently accompanied by an adenocarcinoma component. Because the carcinogenic parthway and genetic alterations remain unclear, we investigated the histogenesis of the tumor by histopathological and p53 gene analysis. METHODS: The materials were 68 gastric endocrine cell carcinomas and 30 carcinoid tumors, which were resected from 93 Japanese patients for histopathological and immunohistochemical investigation. We also analyzed the concordance of p53 mutational status between the associated adenocarcinoma and endocrine cell carcinoma components, using microdissection and direct sequencing techniques. RESULTS: An adenocarcinoma component was associated with 70.6% (48/68) of endocrine cell carcinomas, of which 42 (87.5%) were of well- to moderately differentiated type, while 36 of these 42 (85.7%) demonstrated histological continuity with the endocrine cell carcinoma components. Overexpression of p53 protein was observed in 58.8% (20/34) of cases. Common p53 mutational status between the two components was revealed in 73.3% (11/15) of cases analyzed. In contrast, carcinoid tumors did not exhibit p53 protein overexpression (0/15) or gene mutation (0/5). CONCLUSIONS: These data suggest that gastric endocrine cell carcinomas predominantly arise from endocrine precursor cell clones occurring in preceding adenocarcinoma components (particularly the differentiated type), transforming into endocrine cell carcinoma during rapid clonal expansion under the influence of p53 gene alteration. Endocrine cell carcinoma of the stomach is characterized by endocrine differentiation and aggressive biological behavior, and is frequently accompanied by an adenocarcinoma component. Because the carcinogenic pathway and genetic alterations remain unclear, we investigated the histogenesis of this tumor by histopathological and p53 gene analysis.

Adenocarcinoma↗

PubMed1978

Sequential differentiation of intestinal endocrine cells in the fetal mouse.

The duodenum and ileum of 15 to 18-day old Swiss ICR mouse embryos were studied with the electron microscope to follow the differentiation of endocrine cells. Endocrine cells were classified on purely morphological characteristics. EC cells appeared at 16 days of gestation in both segments. At the same stage G cells were seen in the duodenum and K cells in the ileum. ECL, and S cells were identified in the duodenum at 17 days. Finally, D cells were seen at 18 days of gestation in the duodenum and ileum. With the electron microscope, endocrine cells were not identified in the small intestine of the mouse before the formation of villi.

Animals↗

PubMed1989

Intestinal endocrine cells in radiation enteritis.

In this study, the intestinal endocrine cells were investigated in 13 surgical specimens affected by radiation enteritis. Endocrine cells were studied by means of Grimelius' silver staining and immunostaining for chromogranin, a general marker of endocrine cells. Positively stained cells were quantified by counting their number per unit length of muscularis mucosa. Results in radiation enteritis were compared with matched control specimens by using Student's t test. Chromogranin immunostaining showed a statistically significant increase of endocrine cells in radiation enteritis specimens compared with controls both in small and large intestine (ileum, 67.5 +/- 23.5 cells per unit length of muscularis mucosa in radiation enteritis versus 17.0 +/- 6.1 in controls; colon, 40.9 +/- 13.7 cells per unit length of muscularis mucosa in radiation enteritis versus 9.5 +/- 4.1 in controls--p less than 0.005 in both instances). Increase of endocrine cells was demonstrated also by Grimelius' staining; however, without reaching statistical significance. It is not clear whether or not the increase of endocrine cells in radiation enteritis reported in this study is caused by a hyperplastic response or by a sparing phenomenon. We should consider that increased endocrine cells, when abnormally secreting their products, may be involved in some of the clinical features of radiation enteropathy. In addition, as intestinal endocrine cells produce trophic substances to the intestine, their increase could be responsible for the raised risk of developing carcinoma of the intestine in long standing radiation enteritis.

APUD Cells↗

PubMed2002

c-Myc controls proliferation versus differentiation in human pancreatic endocrine cells.

Using immortalized human pancreatic endocrine cell lines, we have shown previously that differentiation into hormone-expressing cells requires cell-cell contact acting in synergy with the homeodomain transcription factor pancreatic duodenal homeobox-1 (PDX-1). Although differentiation is associated with a decrease in cell proliferation, the mechanisms behind this relationship are not known. Using TRM-6, a delta cell line, and betalox5, a beta-cell line, we show here that cell-cell contact and subsequent endocrine differentiation lead to a down-regulation of the c-myc protooncogene. Overexpression of c-Myc obtained with an inducible c-Myc-estrogen receptor fusion protein results in an increase in cell proliferation and the ablation of hormone expression. Moreover, we show that although c-Myc is expressed in a subset of cells from the human fetal and adult pancreas, it is absent in differentiated endocrine cells. The mechanism by which c-Myc interferes with hormone expression may be through effects on the homeodomain transcription factor PDX-1, as immunostaining for PDX-1 in cells with activated c-Myc revealed a redistribution of PDX-1 from the nucleus to the cytoplasm. These results suggest that c-Myc plays a central role in a cell-cell contact-mediated switch mechanism by which cell division vs. differentiation in endocrine cells is determined.

Adult↗

PubMed2002

Adenosine-regulated cell proliferation in pituitary folliculostellate and endocrine cells: differential roles for the A(1) and A(2B) adenosine receptors.

A(1) and A(2) adenosine receptors have been identified in the pituitary gland, but the cell type(s) on which they are located and their effects on pituitary cell growth are not known. Therefore, we analyzed the expression of A(1) and A(2) receptors in primary rat anterior pituitary cells, two pituitary folliculostellate (TtT/GF and Tpit/F1) and two pituitary endocrine (GH(3) and AtT20) cell lines, and compared their effects on cell proliferation. In anterior pituitary and folliculostellate cells, adenosine and adenosine receptor agonists (5'-N-ethylcarboxamidoadenosine, a universal agonist, and CGS 21680, an A(2A) receptor agonist) stimulated cAMP levels with a rank order of potency that indicates the presence of functional A(2B) receptors. This stimulation, however, was not observed in either GH(3) or AtT20 cells, where adenosine and the A(1) receptor agonist 2-chloro-N(6)-cyclopentyladenosine inhibited VIP/forskolin-stimulated cAMP production. Expression of A(2B) and A(1) receptors in the folliculostellate cells and that of the A(1) receptor in the endocrine cells were confirmed by RT-PCR, immunocytochemistry, and ligand binding. Adenosine and 5'-N-ethylcarboxamidoadenosine dose-dependently (10 nM to 10 microM) stimulated growth in the folliculostellate, but not in the endocrine, cells, whereas in the latter, 100 microM adenosine and 2-chloro-N(6)-cyclopentyladenosine inhibited cell proliferation by slowing cell cycle progression. These data highlight the differential expression of A(1) and A(2B) adenosine receptors in pituitary cells and provide evidence for opposing effects of adenosine on pituitary folliculostellate and endocrine cell growth.

Adenosine↗

PubMed1991

Morphometric and immunohistochemical study on the endocrine cells of pancreatic transplants.

The endocrine cells of embryonic pancreatic tissue fragments transplanted into the anterior eye-chamber of rats for 74 days were investigated immunohistochemically and morphometrically and the results obtained were compared with that of normal tissue. Four types of endocrine cells were identified and their distribution was as follows: insulin: 42-52%, glucagon: 11-28%, somatostatin: 4%, and pancreatic polypeptide-positive cells: 3-6%. Their size in square micrometer were as follows: 153, 110, 38 and 51. The area, number, distribution and topography of these endocrine cells with regard to each other did not differ significantly from that of normal tissue. The area of each islet and their cell population vary considerably both in normal and transplanted pancreas.

Animals↗

PubMed1992

An immunocytochemical study of endocrine cell development in the early fetal guinea pig pancreas.

The presence of insulin, glucagon, pancreatic polypeptide, and somatostatin containing cells and their ontogenic changes were investigated immunocytochemically in the early fetal pancreas of the guinea pig (Days 25-40). In the earliest tissues examined (Day 25 and Day 30) brightly staining glucagon cells were the most predominant endocrine cell population, followed by slightly fewer and weaker staining pancreatic polypeptide cells. Insulin and somatostatin immunoreactive cells were less numerous. At Day 25 all endocrine cells were located within the pancreatic tubules where some glucagon cells also coexpressed insulin. Similar dual immunoreactivity was present at Day 30. At Day 25 some of the pancreatic polypeptide cells also showed coexpression of somatostatin which persisted until Days 35-40. At these later stages insulin and somatostatin cells were increasingly frequent. Glucagon and pancreatic polypeptide cells were also conspicuous. The four endocrine cell types were found either in the pancreatic tubules or in the developing islets where they began to acquire an adult-like topographic distribution. These studies in the fetal guinea pig show that the four islet hormonal cells cytodifferentiate from an early stage. A small proportion of endocrine cells coexpress either insulin and glucagon or pancreatic polypeptide and somatostatin.

Animals↗

PubMedDate not supplied

Endocrine cells in gastric carcinoma and adjacent mucosa. An immunohistochemical and ultrastructural study.

Endocrine cells are often found in human gastric carcinoma and may be recognized by the immunoreactivity of their chromogranin A, peptides and biogenic amines content. Anti-chromogranin A was used to investigate the morphology of endocrine cells using light and electron microscope immunohistochemical techniques. The hormone content of endocrine cells was examined in both tumour tissue and tumour-adjacent mucosa. It was found that the endocrine cells in tumour tissue were malignant, often had amphocrine differentiation and did not resemble a normal cell type. The hormone content of endocrine cells in tumour tissue seldom corresponded to the hormonal content of endocrine cells in tumour-adjacent mucosa. In intestinal-type carcinoma and in some parts of diffuse-type gastric carcinomas, endocrine cell hyperplasia and an alteration of the differentiation in the tumour-adjacent mucosa were discovered. The distribution of endocrine cells in the tumour tissue was different in both types of gastric carcinoma. The results reported here suggest that endocrine cell differentiation of malignant endocrine cells in human gastric carcinoma develops in a different way from that of endocrine cells in tumour-adjacent mucosa, and as a result, diverse hormonal products may appear in tumour tissue.

Aged↗

PubMed1988

A case of multiple carcinoid tumors of the rectum with extraglandular endocrine cell proliferation.

A case of multiple carcinoid tumors of the rectum with numerous proliferations of extraglandular endocrine cells is reported. The patient was 52-year-old man with five polypoid lesions in the rectum. The resected rectum contained five macroscopic carcinoid tumors, 36 microcarcinoids, and innumerous extraglandular endocrine cell proliferations. Endocrine cell microproliferations, in their early stage consisting of one to 15 micronests, were mainly located within the bundles of muscularis mucosae, having no contact with mucosal glandular structures. All of the immunohistochemically examined proliferations of extraglandular endocrine cells contained S-100 protein-positive dendritic cells, and some endocrine cells coexisted with submucosal ganglion cells. In contrast, there was no increase in intraglandular endocrine cells. The origin of rectal carcinoid tumor may be the extraglandular endocrine cells, a distinct compartment of mucosal endocrine cells of the rectum.

Carcinoid Tumor↗

PubMed1984

[Existence of cytoplasmic bridges between gastric endocrine cells].

The fine structure of endocrine cells of the rat's stomach has been studied. 3 of 25 animals displayed structural formations, which could be interpreted as "cytoplasmatic bridges" between endocrine cells of the acid-producing part of the stomach. In these areas no plasmalemma existed between cells, and endocrine granules and vacuoles were present. There is no cytophysiological evidence of intercellular transport of such big organoids. Possible causes and conditions of formation of the above structures are discussed.

Animals↗

PubMed1996

Perinatal changes in bovine SEGI's caps with special reference to their endocrine cells migrating into the lamina propria.

Large aggregations of endocrine cells at the top of villi in the upper small intestine, discovered by SEGI (1935) in human fetuses and hence called SEGI's caps, have been known to occur also in bovine and porcine fetuses. Using bovine fetuses and newborns, this study aimed to clarify the fate of and changes in the SEGI's cap during the perinatal period. Immunocytochemistry was performed for CgA and PGP 9.5 as markers of the endocrine and nervous elements concerned. In the second trimester in bovine fetuses, numerous endocrine cells were confirmed, by CgA immunocytochemistry, to gather in the epithelium on the top of almost every duodenal villus, either in a single layer or accumulating in a rounded cell mass. They persisted until birth, though decreasing in number during the third trimester. In these fetal periods the endocrine cells came to be invaginated into the lamina propria, and to be separated from the epithelium. They were attached by nerve fibers and shifted to the base of the villi and to the intercryptal tissue. The endocrine cell aggregations at the villous tips rapidly disappeared within three days after birth. The intraepithelial endocrine cells (paraneurons) decreased in their immunoreactivity for CgA after they shifted into the lamina propria, whereas they increased in their immunoreactivity for PGP 9.5 while descending the villous interstitium. Using immunocytochemistry for PGP 9.5, we were able to trace the descent of the endocrine cells in association with nerve fibers. Microscopic images were obtained supporting the possibility that the endocrine-type cells eventually might be taken up by the intramural plexuses of Meissner and Auerbach. Furthermore, the fetal and perinatal intestine revealed enlarged solitary endocrine cells and authentic neurons, as well as their intermediate types, in the villous and intercryptal interstitium. The present results indicate that the SEGI's caps in cattle are best developed in the second trimester of the fetal life, and do not support a hypothesis that the endocrine sensor cells in the caps principally function at the time of birth, especially for responding to the advent of colostrum. The endocrine or paraneuronal elements of the SEGI's cap appear to migrate into the interstitium to obtain more neuron-like features. A possibility that they may be incorporated in the intramural ganglia and further be transformed into neurons awaits further investigation.

Animals↗

PubMed1977

[Endocrine cells of the esophageal glands].

Distribution of endocrine cells in the human oesophagus was studied histochemically. Large amount of endocrine cells was discovered in terminal parts and excretory ducts of the cardial glands. Endocrine cells of the oesophageal cardial glands are represented, at least, by three types: argentaffine, argyrophil in the reactions of Grimelius and Sevier, Munger and argyrophil in the reaction of Grimelius only. The amount of argentaffine cells in the oesophageal cardial glands was observed to be 5 times as large as that of in the gastric cardial glands. The reason is evidently in functional difference of the oesophageal and gastric cardial glands. The endocrine cells were absent in the mucous glands of the oesophagus.

Cardia↗

PubMed1997

Application of computer image analysis in endocrine cell quantification.

Computer image analysis was applied for quantifying endocrine cells by using an automatic standard sequence analysis operation. Two parameters were used, namely the number of cells per mm3 of epithelial cells and the cell secretory index (the volume of the immunoreactive secretory granules per cell). The first indicates the variation in the anatomical peptide-producing unit and the second the synthesis and secretion activity of the cell. The endocrine cells chosen in this study were chromogranin-immunoreactive cells and secretin-immunoreactive cells in the human duodenum. The measurements were made by five different investigators with different backgrounds in order to evaluate the effect of the intra- and inter-individual variation. This study showed that the intra- and inter-individual variation had no impact on the results. Comparisons with the classical point-counting method considered to be easy and most efficient in volumetry showed that the present approach is between two and three times faster and less strenuous for the performer. It is concluded that this approach seems to be suitable for adaptation in morphometric studies when information is required about the changes in the number of endocrine cells and about changes in secretory activities.

Adult↗

PubMed2001

IMPAN cells: a pancreatic model for differentiation into endocrine cells.

It is currently believed that pancreatic progenitor or stem cells exist in the ductal cell population and that these cells have the ability to be grown and differentiated into endocrine cells for the treatment of diabetes. In this study, we have examined this potential in IMPAN (Immortalized Pancreatic) cells. These cells are derived from the adult H-2K(b)-tsA58 transgenic mouse. We observed an increased mRNA expression of insulin, proendocrine gene neurogenin 3, and beta-cell transcription factor Pdx1 when the cells were grown on bovine collagen I gels. The induction profile of these three genes was similar under the tested conditions. No glucagon or other endocrine-specific transcription factors were detectable. Application of GIP, GLP-1 derivative NN2211, and activin-A/betacellulin to IMPAN cells in normal culture did not lead to endocrine differentiation. In conclusion, it appears that the ability of IMPAN cells to mature to endocrine cells is limited.

Activins↗

PubMed1983

Extraepithelial intraneural endocrine cells as starting-points for gastrointestinal carcinoids.

Endocrine cells can be demonstrated by light- and electron microscopy in the lamina propria of the mucosa of the appendix. They are always in direct contact with a nerve fibre. The endocrine cell (type EC1 and EC2 cell) and the polyaxonal non-myelinated nerve fibre are separated from the interstitial connective tissue by a common continuous basal lamina. The term "ECC-NF complex" ("EC cell-nerve fibre complex") is suggested by the authors to describe this morphological unit. The intraneural endocrine cells may be derived from neuroendocrine-programmed ectoblasts (Pearse, 1977). The electron microscopic demonstration of these "ECC-NF complexes" in carcinoid tumours of the appendix and of similarly structured "eC-NF complexes" ("endocrine cell-nerve fibre complexes") in carcinoids of the rectum allows us, following the demonstration of small nerve fibres within carcinoids of the appendix, caecum and rectum (and bronchus) to propose a hypothetical pathogenesis of gastrointestinal carcinoid tumours from these intraneural endocrine cells. Carcinoid tumours may develop by proliferation of the intraneural endocrine cells with microcarcinoids as intermediate stages. In this way the histogenesis of the carcinoids is located a priori in the subepithelial stroma. Nerve fibres are morphological markers of this proposed mechanism. Assuming a neuroectodermal cytogenesis for the intraneural endocrine cells we therefore also postulate a histogenesis of the carcinoids from the neuroectoderm.

Appendiceal Neoplasms↗

PubMed1987

Induction of a neural phenotype in a serotonergic endocrine cell derived from the neural crest.

The thyroid parafollicular cell is an endocrine cell derived from the neural crest that stores 5-hydroxytryptamine (5-HT). In common with serotonergic neurons, but in contrast to 5-HT-storing cells that are not neurectodermal derivatives, parafollicular cells also contain a specific 5-HT binding protein. Despite this similarity to serotonergic neurons, parafollicular cells in situ were found to express an endocrine phenotype with few neural characteristics. Thus, the cells costore 5-HT with calcitonin, not calcitonin gene-related peptide (CGRP), which is the product of the calcitonin gene expressed in neurons, and they do not contain neurofilaments. The ability of adult parafollicular cells to respond to microenvironmental perturbations by expressing neuronal characteristics was examined. Sheep thyroid glands were dissociated, and parafollicular cells were purified by affinity chromatography. The purified parafollicular cells were grown in culture on a variety of substrates in the presence or absence of the beta subunit of nerve growth factor (beta-NGF). Parafollicular cells survived in culture for at least a week but retained a roughly spherical shape. Nevertheless, a subset of the cultured parafollicular cells began to display CGRP immunoreactivity. The addition of beta-NGF to the cultured parafollicular cells induced a number of them to extend neurites and increased the proportion of cells in which CGRP immunoreactivity could be found. Neurite-bearing parafollicular cells appeared not to survive for more than 2 d. While their survival was not enhanced when they were grown on collagen, polylysine, laminin, or reconstituted basal lamina, parafollicular cells that had extended neurites in response to beta-NGF survived for at least a week when cocultured with an explant of aneuronal chick hindgut. The effect of the gut was local and only those neurite-bearing parafollicular cells that were growing in direct contact with the explant survived. The thyroid parafollicular cell therefore resembles another crest-derived endocrine cell, the adrenal chromaffin cell, in being able to manifest neural properties in culture. For the parafollicular cell these neural properties include the processing of RNA encoded by the calcitonin gene to express CGRP and neurite outgrowth in response to beta-NGF.

Animals↗