Cell Renewal in the Gastric Mucosa

Willems, Glenda

doi:10.1159/000197221

Cited by 34 publications

(12 citation statements)

References 35 publications

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“…We have been unable to confirm the very early commencement of mitotic activity as reported by Hunt (7), which is also not to be expected on the basis of recent data concerning the cell cycle time in the rat stomach mucosa (20). It is impossible to estimate to which extend the elevated borders around the lesion are due to contraction in the lesion area or to an active 'piling up' o f epithelial material as a consequence of locally increased mitotic activity.…”

Section: Discussioncontrasting

confidence: 85%

The Epithelium in Healing Experimental Standard Lesions in the Gastric Mucosa of the Rat

et al. 1977

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In a series of experiments in rats, the movement of the advancing sheet of epithelial cells streaming from the border region into the wound bed of standardized defects in the glandular mucosa of the stomach was studied using the light microscope and the scanning electron microscope (SEM). A very high synthetic activity of mucus in gastric lining cells of the border region (with a typical shift in its reaction product towards a more acidly reacting product showing metachromasia with toluidine blue) was observed histochemically, together with a loss of characteristic features of glandular cells in the border region with an increase in mitotic activity. The SEM images enabled a detailed analysis of the advancing epithelial front in its relation to the border regions. Considerable local differences were noted in the moving pattern of the migrating epithelium, possibly in relation with the nature of the base on which it has to move. The lesion of 3 mm diameter appeared to close usually after 10 days; in some instances, however, small epithelial defects were later found which could easily be traced with the SEM.

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Section: Discussioncontrasting

confidence: 85%

The Epithelium in Healing Experimental Standard Lesions in the Gastric Mucosa of the Rat

et al. 1977

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“…Thus, in both models . The cell cycle phase duration (Tc) was estimated following the method described by Willems (Willems, 1972). Percentage of positive mitotic figures refers to the ratio between BrdU labelled and total (labelled + unlabelled) mitosis.…”

Section: Discussionmentioning

confidence: 99%

“…After BrdU administration, the locusts were dissected at 30·min, at 1·h and then every hour until 24·h had elapsed. To determine the cell cycle phases we used the method of Willems (Willems, 1972). This method extrapolates cell cycle duration from the graphical representation of the BrdU labelled/ unlabelled mitosis ratio against time.…”

Section: Cell Cycle Experimentsmentioning

confidence: 99%

“…Using Willems method (Willems, 1972), we represented the ratio (percentage) of BrdU-labelled vs total (labelled + unlabelled) mitosis plotted against the time elapsed from BrdU injection to dissection. The complete cell cycle duration (Tc) was estimated to be 10·h, This time was calculated from the graph by measuring the distance between the two peaks of high percentage BrdU-labelled mitosis (Fig.·7).…”

Section: Cell Cycle Durationmentioning

confidence: 99%

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The regenerative nidi of the locust midgut as a model to study epithelial cell differentiation from stem cells

Illa-Bochaca

Montuenga

2006

Journal of Experimental Biology

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SUMMARY A better knowledge of the regulatory mechanisms involved in stem cell proliferation and/or differentiation could reveal new methods for the treatment of some diseases. Most previous studies in the field of stem cell biology have been carried out on cultured isolated cells. In the case of adult tissue stem cells, mesenchymal bone marrow derived cells have been most widely studied, while the undifferentiated stem cells present in the epithelial tissues are less known. In order to advance further our understanding of epithelial tissue stem cells, new in vivo models are required. The present study focuses on the dynamics of a new and simple model of intestinal epithelial regeneration found in the midgut of the migratory locust, Locusta migratoria (Linnaeus 1758). The locust midgut consists of three cell types: columnar cells, endocrine cells and undifferentiated regenerative clustered cells. The undifferentiated epithelial midgut cells give rise to two other cell types and are located in a nest of regenerative cells known as regenerative niche. We have performed single and continuous bromodeoxyuridine (BrdU) administration experiments to study regeneration niches and their cellular dynamics. Immunocytochemistry and immunofluorescence techniques were used to detect the incorporation of BrdU into regenerative niches and the presence of FMRFamide-like immunoreactivity, as a marker for endocrine cell differentiation. Some isolated label retaining cells (LRC) were observed at the niche base 10-15 days after the final BrdU administration. We propose that these cells are the stem cells of this epithelial tissue. We also calculated the length of the cell cycle phases for a subpopulation of transit amplifying cells within the regenerative niche: G1, 2.5±0.5 h; S,5.5±0.5 h; G2, 0.75±0.25 h; M, 2.5±0.5 h. These amplifying cells will give rise to the columnar epithelial non-endocrine lineage. The differentiation of an endocrine cell from a niche stem cell occurs less frequently and thus leads to a lower proportion of endocrine cells as compared with epithelial columnar digestive cells (up to three endocrine cells per niche). Endocrine cell commitment seems to occur very early in the differentiation process within the niche, as double-labelled BrdU and FMRF endocrine cells have never been found. The only exception is the endocrine cells located in the ampullar region of the midgut, some of which show double immunostaining after long-term chronic BrdU injection. In summary, we have characterized a new and simple animal model of epithelial stem cell regeneration that may be useful for understanding the complex biological process that drives tissue renewal from undifferentiated and uncommitted progenitor cells.

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“…It is hardly probable that reduced new cell pro duction is a primary effect of PGEs. A more likely but hypothetical explanation is that the reduced MI is a secondary phenomenon and a result of a negative feedback from the hyperplastic epithelium [2,9,16,17], If so the primary action of the compound should be to prolong the survival time of gastroin testinal epithelial cells by reducing losses of cells into the lumen and/or slowing of the cell migration time. As expected, such a sec ondary reduction of mitotic activity took place firstly in the antral mucosa, where tro phic changes are most prominent.…”

Section: Discussionmentioning

confidence: 99%

Cell Proliferation of the Rat Gastrointestinal Mucosa after Treatment with E<sub>2</sub> Prostaglandins and Indomethacin

Uribe¹,

Johansson²,

Rubio

1987

Digestion

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The frequency of arrested mitoses after vincristine injection was studied in the gastrointestinal mucosa of rats treated with either natural prostaglandin E₂ (0.2–5.0 mg·kg^-1, b.d.), 15-R-15 methyl prostaglandin E₂ (2 mg•kg^-1, b.d.) or indomethacin (1.0–3.0 mg•kg^-1, b.d.). In addition to the mitotic index, morphometric measurements including the mucosal thickness and the thickness of the proliferative and functional zones of the gastric corpus, antrum and jejunum were performed. Natural prostaglandin E₂, at the highest dose range, reduced significantly the mitotic index in the gastric antrum. Normal values were found in the gastric corpus and jejunum and in the antrum with the lower doses. The mitotic index was unaffected by treatment with 15-R-15 methyl prostaglandin E₂. Natural prostaglandin E₂ produced trophic changes (i.e. increased thickness and/or hyperplasia) in the antrum, functional epithelial zone of the gastric corpus and in the jejunum. More pronounced trophic changes were observed in the mucosa of rats treated with the analogue. Indomethacin reduced the mucosal thickness in all examined epithelia and lowered the mitotic index in the jejunum. It is concluded that the trophic effects of E₂ prostaglandins on gastrointestinal epithelia are not caused by increased production of new cells. The reduced mitotic index observed in the antral mucosa of prostaglandin-treated rats could be secondary to a negative feedback from the hyperplastic epithelium. The antitrophic effects of the prostaglandin-synthesis blocker (indomethacin) indicates that endogenous prostaglandins may participate in the epithelial cell regulation of the gastrointestinal tract.

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Cell Renewal in the Gastric Mucosa

Cited by 34 publications

References 35 publications

The Epithelium in Healing Experimental Standard Lesions in the Gastric Mucosa of the Rat

The Epithelium in Healing Experimental Standard Lesions in the Gastric Mucosa of the Rat

The regenerative nidi of the locust midgut as a model to study epithelial cell differentiation from stem cells

Cell Proliferation of the Rat Gastrointestinal Mucosa after Treatment with E<sub>2</sub> Prostaglandins and Indomethacin

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