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Pathology, Otto-von-Guericke-University, Leipzieger Strasse 44, 39120 Magdeburg, Germany
Department of Medicine II, Klinikum rechts der Isar, Technische Universität München, 81675 München, Germany
Obstetrics and Gynecology, Otto-von-Guericke-University, Leipziger Strasse 44, 39120 Magdeburg, Germany
Department of Pathology, Charité – Universitätsmedizin Berlin, Schumannstrasse 20/21, 10117 Berlin, Germany
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Pathology, Otto-von-Guericke-University, Leipzieger Strasse 44, 39120 Magdeburg, Germany
Department of Medicine II, Klinikum rechts der Isar, Technische Universität München, 81675 München, Germany
Obstetrics and Gynecology, Otto-von-Guericke-University, Leipziger Strasse 44, 39120 Magdeburg, Germany
Department of Pathology, Charité – Universitätsmedizin Berlin, Schumannstrasse 20/21, 10117 Berlin, Germany
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Pathology, Otto-von-Guericke-University, Leipzieger Strasse 44, 39120 Magdeburg, Germany
Department of Medicine II, Klinikum rechts der Isar, Technische Universität München, 81675 München, Germany
Obstetrics and Gynecology, Otto-von-Guericke-University, Leipziger Strasse 44, 39120 Magdeburg, Germany
Department of Pathology, Charité – Universitätsmedizin Berlin, Schumannstrasse 20/21, 10117 Berlin, Germany
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Pathology, Otto-von-Guericke-University, Leipzieger Strasse 44, 39120 Magdeburg, Germany
Department of Medicine II, Klinikum rechts der Isar, Technische Universität München, 81675 München, Germany
Obstetrics and Gynecology, Otto-von-Guericke-University, Leipziger Strasse 44, 39120 Magdeburg, Germany
Department of Pathology, Charité – Universitätsmedizin Berlin, Schumannstrasse 20/21, 10117 Berlin, Germany
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secretion in the pancreas and biliary tract, and causes Cl − secretion from human colonic mucosa ( Trimble et al. 1987 , Gullo et al. 1992 , Chey & Chang 2001 ). In addition, NT has been shown to stimulate growth of normal intestinal mucosa in vivo
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Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel
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cm proximal to the ileocecal junction). Each segment was weighed, and mucosa were scraped off using a glass slide and weighed. The mucosal samples were stored at −80 °C for further gene and protein investigation. Crypt cell proliferation and apoptosis
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ABSTRACT
Atrophy of the exocrine pancreas was induced in rabbits by pancreatic duct ligation. Somatostatin concentration and binding in cytosol from rabbit duodenal mucosa were studied after 6 and 14 weeks of pancreatic duct ligation. Somatostatin-like immunoreactivity was significantly increased in the duodenal mucosa in both periods. Scatchard analysis showed a parallel increase in the number of binding sites rather than a change in their affinity. The physiological significance of these findings remains to be clarified.
J. Endocr. (1988) 118, 227–232
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SUMMARY
Immunoreactive gastrin was measured in subcellular fractions of rat gastric mucosa. The sedimentational properties of subcellular gastrin-containing structures were distinct from those of mitochondria. After centrifugation in sucrose density gradients using a zonal rotor, the peak of immunoreactive gastrin was found in 1·17–1·18 g cm−3 density sucrose (1·35 m; 39·5%, w/w). A thermolabile component with 125I-labelled gastrin-binding activity present in gastric mucosal homogenates and fractions was not associated with the gastrin storage vesicles sedimenting in density gradients.
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The finer vascular system of the extra-placental uterine mucosa of the rabbit during oestrus and the early stages of pregnancy and pseudopregnancy was studied by means of the benzidine-nitroprusside blood stain and by injection.
In the oestrous uterus there is a marked mesometrial hyperaemia which intensifies during the early stages of pregnancy and pseudopregnancy.
No spiral arteries nor arterio-venous anastomoses were found in the uterine endometrium.
During the early stages of pregnancy, as the uterine mucosa proliferates, there is an intense growth of new blood vessels, accompanied by a corresponding increase in the amount of blood in the vessels. This occurs throughout the uterus at first, but after 8 days post coitum the increase continues around the conceptus but slows down and finally stops between the conceptuses and in the pseudopregnant horn.
When the trophoblast of the blastocyst wall fuses with the uterine epithelium the fusion areas become well vascularized. It is suggested that this vascularization is stimulated by the invading trophoblast.
The trophoblast actually breaks down the walls of the maternal capillaries and allows the maternal blood to bathe the embryonic syncytium and during the time that this is happening there is a marked leucocytosis around the fusion areas.
The results are discussed in relation to the previous literature and to their possible physiological significance.
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The effects of prolactin on various tissues have been reviewed recently by Sulman (1970). In the search for target receptors of prolactin, the capacities of pigeon crop sac mucosa and of the rat mammary gland to bind labelled prolactin were investigated. Cox (1951) used labelled prolactin for similar studies in mice and found appreciable amounts of radioactivity in the mammary glands but noticed rapid breakdown of the labelled hormone.
For the present study two methods were used: (a) radioactivity was measured in mammary glands of lactating rat mothers 1–12 h after i.v. injection of 125I-labelled prolactin; (b) mucosal proliferation and uptake of radioactivity by the pigeon crop were measured after local injection of 125I-labelled prolactin, 125I-labelled human chorionic gonadotrophin (HCG), 131I-labelled albumin or Na125I. Iodination was carried out according to Greenwood, Hunter & Glover (1963), using Na125I (Amersham) and PS-9 prolactin (N.I.H.)
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Intestinal development is modified by age and nutrition, mediated in part by insulin-like growth factors (IGF-I, IGF-II) and insulin. We have investigated whether expression of IGF-I, IGF-II and insulin receptors (IGF-IR, IGF-IIR and IR; measured by real-time RT-PCR) and binding capacity (Bmax) of IGF-IR, IGF-IIR and IR in the mucosa of the small and large intestine of neonatal calves are modified by age and different feeding regimes. In experiment 1, pre-term (GrP) and full-term (GrN) calves (after 277 and 290 days of pregnancy respectively) were killed immediately after birth before being fed; a further group of full-term calves were fed for 7 days and killed on day 8 of life (GrC(1-3)). In experiment 2, full-term calves were killed on day 8 after being fed first-colostrum for 7 days (GrCmax), colostrum of the first six milkings for 3 days (GrC(1-3)) or milk-based formula for 3 days (GrF(1-3)). Intestinal sites differed with respect to expression levels of IGF-IR (duodenum>jejunum in GrC(1-3); ileum>colon, duodenum> or = jejunum in GrF(1-3)), IGF-IIR (colon>duodenum and ileum in GrN), and IR (lowest in ileum in GrP and CrN; highest in colon in GrC(1-3) and GrCmax). They also differed with respect to Bmax of IGF-IR (ileum and colon>duodenum and jejunum in GrP; ileum and colon>jejunum in GrN; colon>jejunum in GrC(1-3); lowest in jejunum in GrF(1-3)), IGF-IIR (duodenum and colon>jejunum and ileum in GrP; duodenum>ilem and colon>jejunum in GrN; duodenum, jejunum and colon>ileum in GrCmax, GrC(1-3), and GrF(1-3)) and IR (ileum>duodenum, jejunum and colon in GrCmax, GrC(1-3), and GrF(1-3)). There were significant differences between groups in the expression of IGF-IR (GrF(1-3)> GrCmax and GrC(1-3) in ileum), IGF-IIR (GrN>GrP and GrC(1-3) in colon; GrN>GrC(1-3) in jejunum and total intestine), and IR (GrCmax>GrF(1-3) in colon) and in the Bmax of IGF-IR (GrP>GrN in colon; GrCmax>GrF(1-3) in jejunum), IGF-IIR (GrN>GrP in duodenum, ileum and total intestine; GrN>GrC(1-3) in duodenum, ileum, colon and total intestine) and IR (GrN>GrP in total intestine; GrC(1-3)>GrN in ileum and total intestine). In addition, Bmax values of IGF-IR, IGF-IIR and IR were correlated with villus circumference, villus height/crypt depth and proliferation rate of crypt cells at various intestinal sites. There were marked differences in Bmax of IGF-IR, IGF-IIR and IR dependent on mRNA levels, indicating that differences in Bmax were the consequence of differences in posttranslational control and of receptor turnover rates. In conclusion IGF-IR, IGF-IIR and IR expressions and Bmax in intestinal mucosa were different at different intestinal sites and were variably affected by age, but not significantly affected by differences in nutrition. Receptor densities were selectively associated with intestinal mucosa growth.
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ABSTRACT
There is evidence that prolactin (PRL) influences gastrointestinal function. However, the sites at which prolactin exerts these effects are not known. A monoclonal antibody was therefore generated against the rabbit mammary gland prolactin receptor (MAb 218) and used to study the distribution of the prolactin receptor in the rabbit gastrointestinal tract (GIT) by immunohistochemistry. MAb 218 is an IgG 1 κprecipitating antibody which precipitates major affinity cross-linked mammary gland prolactin receptor subunits of molecular masses 45 and 80 kDa. It has an affinity of 0·8 × 109 mol/l for the prolactin receptor and does not react with GH or insulin receptors in precipitation assays. MAb 218 immunoreactivity was observed in classical prolactin target cells such as mammary gland epithelium, and this immunoreactivity was abolished by preincubation of MAb 218 with purified prolactin receptor but not by preincubation with purified GH receptor.
In the GIT, the most intense immunoreactivity was associated with the oesophageal epithelium, chief (zymogenic) cells of the fundic mucosa, pancreatic islets of Langerhans and surface epithelial cells of the duodenum and jejunum. Other specific elements of the GIT were immunoreactive at lower levels or were immunonegative. No immunoreactivity was observed in these locations with a control monoclonal antibody (MAb 50·8) of identical isotype to 218.
To support the immunohistochemical findings, rabbit gastric mucosal membranes were used to show the presence of lactogen-specific binding. Scatchard analysis of 125I-labelled human GH binding to the gastric mucosal membranes with rat prolactin as displacing ligand yielded an affinity constant (K a) of 1·0 ± 0·2 × 109 mol/l with a capacity of 3·5 ± 0·4 fmol/mg protein. Affinity cross-linking and sodium dodecyl sulphate-polyacrylamide gel electrophoresis of the gastric receptor revealed lactogenic hormone-binding subunits of molecular masses 43, 68 and 83 kDa. The 68 kDa subunit was not seen in rabbit mammary gland or ovarian tissue, and may be unique to gastric mucosa.
In conclusion, we have demonstrated the presence of a high affinity lactogenic receptor in specific epithelial cell subpopulations of the GIT. This localization of the prolactin receptor in the GIT will assist in further functional assignment of prolactin to gastrointestinal physiology.
Journal of Endocrinology (1993) 139, 371–382
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SUMMARY
A study was made of the effects of cyclic AMP, theophylline, cycloheximide, puromycin and actinomycin D on the stimulation by angiotensin of fluid transport by sacs of rat colon mucosa.
Cyclic AMP and theophylline, added together or separately, had no effect on fluid transport by colon sacs, suggesting that the stimulation of fluid transport after the application of angiotensin is not mediated through cyclic AMP. Cycloheximide and puromycin (used at concentrations which block colon protein synthesis by 50–90%) had no effect on fluid transport by control colon sacs, but completely blocked the stimulatory response of the colon to angiotensin. In contrast, actinomycin D (at a concentration which significantly inhibits RNA synthesis) did not affect fluid transport in control or angiotensin-stimulated colon sacs. The results are discussed in relation to the possibility that protein synthesis, at the stage of translation, is involved in the action of angiotensin on fluid transport by the colon.
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SUMMARY
The placenta, foetal membranes and uterine mucosa of mice (pregnant for 8–17 days) have been investigated by histochemical methods for NAD-dependent 3β-hydroxysteroid dehydrogenase (3β-HSDH), and for NAD-and NADP-dependent 17α- and 17β-hydroxysteroid dehydrogenases (17α- and 17β-HSDH), 11α- and 11β-hydroxysteroid dehydrogenases (11α- and 11β-HSDH), and 20β-hydroxysteroid dehydrogenase (20β-HSDH).
3β-HSDH was found to be distributed in the trophoblastic giant cells of the first generation with both pregnenolone and DHA as substrates, and in the giant cells of the second generation and of the labyrinth and the endodermal cells of the inverted yolk sac placenta, but only with DHA as substrate.
17α-HSDH and 17β-HSDH, NAD-dependent, were present in both the first and second generation giant cells and in the giant cells of the labyrinth as well as in the endodermal cells of the inverted yolk sac placenta. With NADP as cofactor, 17α-HSDH and 17β-HSDH were weakly positive with all the substrates used in the giant cells of the second generation and of the labyrinth, while NADP-dependent 17β-HSDH was present in the first generation giant cells and in the endodermal cells of the inverted yolk sac placenta but only with oestradiol-17β as substrate.
The histochemical reaction for 11α-HSDH, both NAD- and NADP-dependent, was limited to trophoblastic giant cells of the second generation and of the labyrinth; 11β-HSDH, both NAD- and NADP- dependent, was distributed in the giant cells of the second generation and of the labyrinth, the epithelial cells of the uterine mucosa and the decidua basalis.
The histochemical reaction for 20β-HSDH, NAD- and NADP-dependent, was weakly positive in the giant cells of the first generation only.
