Peptide growth factors: role in epithelial-lamina propria cell interactions.
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Animals↗
Biomedical subjects
C Ciacci
Publications and source records attributed to C Ciacci.
Origins of nephrology: the 17th century. I. The fallacies deriving from examination of the urine according to James Primrose.
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France↗
Transglutaminase changes in intestinal mucosa after experimental small bowel resection in the rat.
The low serum transglutaminase found in various intestinal disorders (celiac disease and IBD) suggested to us to study the serum and mucosal transglutaminase behaviour in an experimental model of small intestine resection in rats to reduce cellular mass and induce enterocyte hyperproliferation in the proximal part left in continuity. Transglutaminase activity in the intestinal mucosa was significantly higher in resected rats than in control and sham operated animals from days 4 (121 +/- 10 v basal 94 +/- 3 mU/g protein, p < 0.01) to 10 (165 +/- 37 mU/g protein, p < 0.05) after surgery; no significant difference was observed at days 12 and 15 (110 +/- 15 and 105 +/- 23 respectively). Both serum alkaline phosphatase activity (partly produced in enterocytes) and serum transglutaminase were significantly lower in resected rats at each time-point beginning at day 6 (208 +/- 34 v 557 +/- 125 UI and 1.55 +/- 0.11 v 3.78 +/- 0.70 mU/ml, p < 0.001 respectively). These data suggest an involvement of transglutaminase in enterocyte proliferation and confirm the association between reduced intestinal mass and low levels of the enzyme in serum.
Alkaline Phosphatase↗
Elevated dietary protein intake impairs the renal hemodynamic response to hyperaminoacidemia in patients with primary glomerular diseases.
We have evaluated the renal hemodynamic response to a mixed amino acid infusion in 7 control subjects and in 8 patients with primary glomerulonephritis (GN). In order to evaluate the role of dietary protein intake in this response, GN patients were maintained for 3 weeks on two separate dietary regimens providing 130 +/- 5 g of protein/day (study 1) and 60 +/- 3 g of protein/day (study 2), respectively. Normal subjects were studied while consuming a free diet. In GN patients, following the reduction in dietary protein intake basal RPF and GFR decreased from 589 +/- 109 to 422 +/- 81 ml/1.73 m2/min (p less than 0.01, vs. study 1) and from 75 +/- 7 to 70 +/- 8 ml/1.73 m2/min (p = NS). Filtration fraction rose from 0.14 +/- 0.02 to 0.19 +/- 0.03 (p less than 0.05). In study 1, during amino acid infusion GFR and RPF did not change significantly from baseline (75 +/- 7 vs. 66 +/- 8 ml/1.73 m2/min at 180 min and 589 +/- 109 vs. 567 +/- 102 ml/1.73 m2/min, respectively). These results are at variance with data obtained in normal controls in whom both GFR and RPF rose significantly following hyperaminoacidemia. In contrast, when dietary protein intake was reduced, a normal renal hemodynamic response to amino acid infusion was restored (GFR went from 70 +/- 8 to 90 +/- 18 ml/1.73 m2/min and RPF from 422 +/- 81 to 517 +/- 90 ml/1.73 m2/min, both p less than 0.05 vs. basal), both absolute and percentage increases were similar to what was observed in controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Regulation of transforming growth factor expression in rat intestinal epithelial cell lines.
Autocrine and paracrine modulation of transforming growth factor expression was assessed in rat intestinal epithelial cell lines designated IEC-6 and IEC-7. Addition of the transforming growth factor alpha (TGF alpha) homologue epidermal growth factor (EGF) to media of subconfluent IEC-6 cells led to autocrine stimulation of TGF alpha expression as well as increased expression of the transforming growth factor beta 1 (TGF beta 1). Increased expression of TGF alpha was maximal between 3 and 6 h after addition of EGF and subsequently declined coincident with increasing level of expression of TGF beta 1, which achieved maximal levels 6 h after addition of EGF and was sustained for more than 12 h. Addition of TGF beta 1 also led to autocrine induction of its own expression coincident with suppression of TGF alpha expression. Addition of TGF beta 1 was associated with increased expression of beta-actin when standardized to a constitutive transcript (GAPDH). Similar responses to addition of EGF and TGF beta 1, were observed in another intestinal epithelial cell line, designated IEC-17. Modulation of expression of TGFs was attenuated when cells were grown on the complex extracellular matrix produced by the Engelbreth-Holm-Swarm tumor (Matrigel), reflecting the baseline induction of TGF beta 1 expression when compared to IEC-6 and IEC-17 cells maintained on plastic. These observations suggest that expression of TGFs is controlled by autocrine mechanisms in intestinal epithelial cell lines and proliferation stimulated by TGF alpha may be initially self-reinforcing but ultimately downregulated by induction of TGF beta 1.
Actins↗
Low serum transglutaminase in patients with intestinal lymphoma and alpha-chain disease.
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Humans↗
Altered renal tubular function in men with high erythrocyte sodium-lithium countertransport.
The renal fractional excretion of uric acid was determined for both a habitual diet and an NaCl-restricted diet in two groups of untreated subjects with low (117-207 mumol per litre of cells per h) and high (373-598 mumol per litre of cells per h) erythrocyte Na-Li countertransport identified in a population-based survey of middle-aged male workers. The group with high Na-Li countertransport had a higher mean blood pressure (P less than 0.05); this group also had a significantly reduced fractional excretion of uric acid with the NaCl-restricted diet even after adjustment for the difference in blood pressure (P less than 0.03). These findings are compatible with an abnormality in kidney tubular function and possibly in the renal handling of sodium in subjects with elevated erythrocyte Na-Li countertransport.
Biological Transport↗
Human serum transglutaminase and coeliac disease: correlation between serum and mucosal activity in an experimental model of rat small bowel enteropathy.
Transglutaminase (TG) activity is increased in the mucosa of patients with coeliac disease. Among 18 patients with untreated coeliac disease we have found a significant decrease (p less than 0.001) in serum levels of TG activity (0.72 (0.23) mU/ml). There was no significant differences between 16 treated coeliacs (1.24 (0.28) mU/ml) and 30 normal controls (1.63 (0.42) mU/ml). To evaluate the connection between serum and mucosal TG activity we used the experimental model of methotrexate induced acute hypoplastic enteropathy in the rat. Transglutaminase activity was unchanged in serum and mucosa 24 and 48 hours after MTX administration, but increased in mucosa (2.606 (0.95) v basal 0.207 (0.026) mU/mg protein, p less than 0.001) and significantly decreased in serum at 72 hours (2.08 (0.38) v basal 5.56 (1.50) mU/ml, p less than 0.001) during intestinal cell proliferation. Activity of the enzyme in the mucosa and serum returned to baseline levels within 120 hours. This experimental animal model helps to explain the data of TG activity in human intestinal mucosa and serum reported in this study. Results are mean (SD).
Animals↗
Behaviour of transglutaminase activity in intestine of starved and refed rats.
Starvation causes an intestinal mucosa atrophy which is greater in jejunum than in ileum. Hypoplasia is promptly reversed by refeeding. Transglutaminase (TG) has been controversially implicated in cell proliferation and its role in intestine is not defined. We investigate, by the above described model, the behaviour of TG in proximal and distal small bowel as well as in colon of rats after 4 days of starvation and at day 1, 2, 3, 4, 5, 7 and 10 of refeeding. Our results emphasize a significative reduction of TG in small bowel induced by starvation (day 0) and a prompt recovery of the enzyme activity after refeeding; furthermore, in the first intestinal tract TG activity reaches from day 2 to day 5 values which are significantly higher than basal. Four days of starvation do not affect TG in colon. In conclusion, our study demonstrates that in rats high values of TG activity are coincident with the intense proliferative phase in small intestine subsequent to starvation atrophy.
Animals↗
Transglutaminase activity along the rat small bowel and cellular location.
A recent report indicates a relationship between human transglutaminase (TG) jejunal mucosa activity and celiac disease. We investigated the enzyme distribution along six consecutive small bowel segments of mucosa and tested TG activity on brush border membranes obtained from whole mucosa homogenate in Wistar rats. TG activity was significantly present in jejunal mucosa even if mostly detected in the distal part of small intestine. Our study indicates highest enzymatic activity in the subcellular fraction containing organelles and cellular membranes (66.8%) while a 7% activity was associated with the brush border fraction.
Animals↗
Postheparin plasma diamine oxidase in subjects with small bowel mucosal atrophy.
Diamine oxidase (DAO) is an enzyme whose low plasma values are enhanced by an intravenous injection of heparin, which releases the enzyme from the enterocytes of the villous tips. In 20 normal controls and 15 untreated subjects affected with an overt malabsorption syndrome and subtotal atrophy shown by Crosby jejunal mucosa biopsy (12 suspected celiac disease and three small bowel lymphoma), plasma diamine oxidase was assayed, over 2 hr following an intravenous bolus of 15,000 IU heparin. Plasma postheparin DAO concentrations and the corresponding values of the area under curve, expressed as units/ml X min (mean +/- SD), were significantly lower in the patients (celiac sprue: 138 +/- 62; lymphoma: 83 +/- 42) compared to normals (481 +/- 104). DAO area values were well correlated (r = 0.81; P less than 0.001) with 24-hr fecal fat excretion but not with xylosuria. Our data suggest that postheparin plasma DAO assay may be useful to detect and quantitate small bowel mucosal atrophy in patients with malabsorption syndromes.
Adolescent↗
Postheparin plasma diamine oxidase increases in patients with coeliac disease during gluten free diet.
An intravenous injection of heparin releases diamine oxidase (DAO) from villous tip enterocytes. In a previous study, we found that postheparin plasma DAO (PHD) values were significantly lower in patients with malabsorption syndrome and small bowel atrophy at jejunal biopsy than in normal subjects. In this study we performed the PHD test in 14 coeliac patients before and after three and six months of gluten free diet to show whether the enterocytes maturing processes induced by the diet joined with enhanced PHD values and to assess the clinical usefulness of this test. In all subjects jejunal biopsy carried out after six months showed a partial but consistent histological recovery. The clinical status, xylosuria and daily faecal fat excretion improved progressively and there was a significant increase (p less than 0.001) in mean PHD activity that reached the normal range after three months. After six months a further slight increase of the mean PHD value was recorded. These data indicate that PHD values rise together with the improved intestinal absorptive functions of coeliac patients on gluten free diet and that this test is a useful tool in monitoring recovery of the small bowel mucosa.
Adult↗
[Morpho-functional evaluation of the small intestine patients with Crohn disease. Enema of the small intestine versus post-heparin plasma diamine oxidase].
Our study was directed not only towards the diagnosis of small bowel Crohn's disease, but especially to a quantitative analysis, for a correct therapeutical approach. This experimental trial is based on the relationship between radiological evidence, measured during small bowel enema, and the seriousness of the morphological and functional damage to the intestinal mucosal membrane, evaluated with a post-heparin diamine-oxidase activity test. With this method we studied 35 selected patients; 16 of them were affected by the disease with an exclusive localization in the small bowel and 5 have been considered separately, because 3 patients had already been operated and the other 2 showed different localizations. In our results, the two parameters were not constantly related to each other. In other words the enema's morphological data sometimes do not accord with the mucosal membrane integrity index expressed by the enzyme. Anyway the importance of this study is the attempt of making an objective comparison between an anatomic situation and its functional consequence. These aspects have a great significance in Crohn's disease.
Amine Oxidase (Copper-Containing)↗
Metabolic fate of plasma diamine oxidase: evidence of isolated and perfused rat liver uptake.
After injection of an intravenous bolus of heparin (15,000 IU) in two groups of subjects, 10 normal volunteers and 6 subjects with external biliary drainage, blood and urine samples were collected; in the latter group bile samples were collected also. All samples were assayed for diamine oxidase (DAO). Persistently high values of this enzyme were found in plasma of both populations after heparin stimulation, while no increase in enzymatic activity was detected in bile and urine. In order to confirm and support the hepatic clearance of DAO, liver uptake of the enzyme derived from porcine kidney, human plasma and human placenta was studied by perfusion of isolated rat liver. Disappearance curves of the enzyme derived from three different sources showed a prompt liver uptake: activity decreased by about 50% in 10 min (endocytic uptake) and a slower but constant reduction during the remaining 110 min of perfusion was observed. These data suggest the hypothesis of liver metabolism of plasma DAO.
Adult↗
Plasma diamine oxidase (DAO) and heparin.
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Amine Oxidase (Copper-Containing)↗
Diamine oxidase in rat small bowel: distribution in different segments and cellular location.
Diamine oxidase (DAO) is an enzyme with high activity found in the small bowel mucosa of the rat and man, and only with very low activity in all other tissues. The present study was designed to investigate the enzymatic distribution along 8 consecutive small bowel segments of mucosa and to test the DAO concentration on brush border membranes obtained from whole mucosal homogenate in Wistar rats. Our data document that DAO activity is mainly distributed in intermediate and distal small bowel segments and is not significantly associated with enterocyte brush border.
Amine Oxidase (Copper-Containing)↗
Bacterial killing by Mytilus hemocyte monolayers as a model for investigating the signaling pathways involved in mussel immune defence.
The signaling pathways involved in mussel immune defence were investigated utilizing a model of killing of Escherichia coli by Mytilus galloprovincialis hemocytes in a co-culture setting. In particular, the role played by different mitogen activated protein kinases (MAPKs) and by the production of eicosanoids were investigated utilising specific cell permeant, pharmacological enzyme inhibitors. Hemocyte pretreatment with the p38 MAPK inhibitor SB203580 significantly reduced bacterial killing, whereas PD98059 (an inhibitor of ERK--extracellularly regulated kinase--MAPK activation) had no significant effect. Wortmannin also inhibited bacterial killing, indicating a crucial role for PI3-kinase activation in the immune response. Killing of E. coli was also reduced by inhibitors of both PLA2 and cyclooxygenase activities, indicating that eicosanoid production is involved in mediating the response to bacterial challenge. The results demonstrate that bacterial killing by mussel hemocytes is particularly sensitive to inhibitors of the key steps involved in the transduction of bacterial signals into the host cell. Moreover, these data indicate that the hemocyte bactericidal activity can be suitably utilized not only for identifying the signaling pathways involved in the response to bacterial infection, but also as a potential investigative-toxicology model to test drugs and contaminants for their effect on the overall mussel immune defence.
Animals↗
Sevelamer worsens metabolic acidosis in hemodialysis patients.
BACKGROUND: Sevelamer hydrochloride, a major phosphate binder for patients on maintenance hemodialysis (MHD) is associated with reduced serum bicarbonate concentration due to hydrochloric acid release in the gut and to the binding of short chain fatty acids in the large intestine. Since metabolic acidosis can be deleterious, a study was devised to compare the time course of serum bicarbonate concentration during treatment with sevelamer hydrochloride or calcium carbonate. METHODS: Sixteen well nourished patients on MHD who were in excellent clinical conditions and achieving target levels for blood pressure (BP) and hemoglobin (Hb), while on a protein intake of 1.1g/kg body weight (bw), were enrolled in the study. After a 2-week washout period, the patients were divided into two groups, each consisting of eight patients, and randomized either to 24 weeks of sevelamer followed by 24 weeks of calcium carbonate (group A) or to 24 weeks of calcium carbonate followed by 24 weeks of sevelamer (group B). Protein intake, n-protein catabolic rate (nPCR), serum concentrations of calcium, phosphate, calcium x phosphate (Ca x P) product, bicarbonate, intact parathyroid hormone (iPTH) and albumin were monitored. Time course changes in serum bicarbonate concentrations in relation to short and long dialytic intervals (48 vs. 72 hr) were also investigated. RESULTS: Both sevelamer and calcium carbonate effectively controlled serum phosphate and the Ca x P product. During calcium carbonate treatment plasma phosphate concentrations were significantly below those of patients on sevelamer. Plasma bicarbonate concentration fell within target DOQI values during calcium carbonate administration both in group A and in group B, a goal which was not achieved under sevelamer administration. After a long dialytic interval in patients on sevelamer, serum bicarbonate concentration averaged 17.3 +/- 1.1 mEq/L, whereas it averaged 21.1 +/- 0.7 mEq/L in patients on calcium carbonate (p<0.01). Finally, a 24-week sevelamer administration caused a statistically significant (p<0.05) reduction (0.8 g/dL) in serum albumin concentration, without affecting iPTH. Taken together, these results indicate that sevelamer worsens metabolic acidosis, which needs to be corrected.
Acidosis↗