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A Stallmach

Publications and source records attributed to A Stallmach.

At least 73 records · Page 4Linked to original sources
PubMed1995

Crypt-villus differentiation reflected by lectin and protein binding to rat small intestinal brush border membranes.

To compare differentiation along the crypt-villus axis in adult rats with changes observed in postnatal maturation with respect to binding capacities for lectins and food proteins, crypts and villi were isolated by in vivo perfusion and in vitro incubation. Brush border membranes were prepared from adults and newborns, and binding of 125I-labeled lectins and food proteins was assessed by airfuge ultracentrifugation. Crypt and villus membrane protein patterns looked almost identical, unlike newborn membranes. Considerable shifts in lectin binding to membranes were observed during postnatal maturation, but not in crypt-villus differentiation. For instance, fucose-specific lectin binding patterns in both preparations resembled the general adult mode. Contrary to differences in food protein binding between newborn and adult membranes, food protein binding did not show a consistent significant difference between membranes of crypt and villus origin in adult animals. In conclusion, membrane differentiation along the crypt-villus axis was found to follow a pattern dissimilar from neonatal maturation as far as protein and carbohydrate composition and food protein binding were concerned.

Aging↗
PubMed1995

Expression of CD44v6 is associated with cellular dysplasia in colorectal epithelial cells.

There is increasing evidence that the expression of variants of the glycoprotein CD44 is related to the invasive and metastatic potential of tumour cells. By in situ hybridisation, we analysed the cellular expression of human homologues of a rat metastasis-associated CD44 variant v6 in invasive and non-invasive colorectal neoplasia and normal colonic mucosa. No specific hybridisation signals could be detected in epithelial cells of the normal crypt (n = 10). In contrast, we found moderate epithelial hybridisation signals in adenomatous polyps of mild dysplasia (n = 6). Adenoma cells of moderate or severe dysplasia (n = 7) showed increased hybridisation signals compared to mildly dysplastic adenomas (P < or = 0.01). We could not demonstrate significant differences in CD44v6 transcript levels between cells of dysplastic adenoma and primary adenocarcinoma (n = 11) (P > or = 0.05). Furthermore, we were not able to demonstrate a significant difference between primary and metastatic tumours (n = 7) (P > or = 0.05). However, there was a significant difference between metastatic carcinoma and adenomas with advanced dysplasia (P < or = 0.01). Our data demonstrate that significant transcriptional expression of CD44v6 is not confined to invasive tumour cells, but is already detectable in cells of adenomatous polyps showing mild dysplasia. The results of this study show a close relationship between cellular dysplasia and steady state levels of CD44 variant v6 transcripts in colorectal neoplasms.

Adenocarcinoma↗
PubMed1995

[Recurrent Crohn disease--definition and diagnosis].

Recurrence in Crohn's disease is a frequently encountered problem in the history of this chronic incurable disease. A number of studies have shown different recurrence and reoperation rates, which is partly due to different definitions and diagnostic strategies. 'Surgical relapse' as defined as reappearance of disease activity in operated patients, 'clinical relapse' after conservatively induced remission or 'endoscopical recurrence' with new pathological changes in the operated gut may be differentiated. The different definitions of recurrence are discussed and diagnostic procedures like endoscopical, laboratory or radiological methods are explained.

Colonoscopy↗
PubMed1994

Increased fibronectin-receptor expression in colon carcinoma-derived HT 29 cells decreases tumorigenicity in nude mice.

BACKGROUND/AIMS: Following malignant transformation, epithelial cells of colorectal carcinomas, unlike normal colonic epithelial cells, no longer express the alpha 5 beta 1 fibronectin receptor. We hypothesized that the loss of alpha 5 beta 1 expression might facilitate the tumorigenicity of transformed colonic cells. METHODS: To examine this hypothesis, we established subclones of the human colon adenocarcinoma cell line HT 29, which differ in their fibronectin receptor expression and tested their tumorigenicity in nude mice. RESULTS: Our data indicate that the capacity to form tumors in nude mice after subcutaneous injection was significantly lower for alpha 5-positive than for alpha 5-negative cell clones. In addition, tumors from clones expressing no detectable levels of alpha 5 beta 1 grew rapidly, whereas tumors expressing elevated levels of fibronectin receptor grew slowly. Despite similar rates of adhesion to fibronectin for alpha 5-positive and alpha 5-negative cell clones in vitro, deposition of fibronectin in tumor-surrounding stroma was increased in tumors derived from alpha 5-positive cells. CONCLUSIONS: Our results indicate that an increase of the alpha 5 beta 1-mediated interaction of malignant cells with the extracellular matrix may be responsible for decreased tumorigenicity of malignant transformed cells in colorectal carcinomas.

Adenocarcinoma↗
PubMed1993

[Loss of fibronectin receptor expression in malignant transformation of the colon results in increased tumorigenicity of epithelial cells].

Following malignant transformation, epithelial cells of colorectal carcinomas unlike normal colonic epithelial cells do not any longer express the classical alpha 5 beta 1 fibronectin receptor. We speculated that the loss of alpha 5 beta 1 expression may facilitate the tumorigenicity of transformed colonic cells. To examine this hypothesis, we established subclones of the human colon adenocarcinoma cell line HT29 which differ in their fibronectin receptor expression and tested their tumorigenicity in nude mice. Our data indicate that the capacity to form tumors in nude mice after subcutaneous injection was significantly lower for alpha 5 beta 1-positive than for alpha 5 beta 1-negative cell clones. In addition, tumors from clones expressing to detectable levels of alpha 5 beta 1 grew rapidly, while tumors expressing elevated levels of fibronectin receptor grew slowly. Deposition of fibronectin in tumor-surrounding stroma was increased in tumors derived from alpha 5 beta 1-positive cells compared to tumors derived from alpha 5 beta 1-negative cells. Our results indicate that a reduction of the alpha 5 beta 1-mediated interaction of epithelial cells with the extracellular matrix may be responsible for increased tumorigenicity of malignant transformed cells in colorectal carcinomas.

Cell Line↗
PubMed1993

[Indications for different collagen metabolism in Crohn disease and ulcerative colitis].

Very little is currently known regarding the underlying mechanisms involved in the etiology of intestinal strictures in chronic inflammatory bowel disease. The deposition of extracellular matrix components, especially collagens, is thought to play an important role in the etiology of intestinal strictures. The main goal of this study was therefore to investigate the collagen metabolism in patients with inflammatory bowel disease using the in situ hybridization technique. We determined de novo synthesis of the (pro)-collagen mRNA transcripts alpha 1I, alpha 1III, alpha 1IV, alpha 2V as well as the collagen degrading enzyme mRNA transcripts collagenase type I and IV in Crohn's disease and ulcerative colitis and compared the rate of expression semiquantitatively to healthy controls. We found a significant increase of all (pro)-collagen transcripts tested in Crohn's disease and ulcerative colitis as compared to healthy control tissues, indicating an increased de novo synthesis of all collagens in both inflammatory bowel diseases. However, we observed a significant difference in the expression of the collagenase mRNA transcripts between Crohn's disease and ulcerative colitis. Compared to healthy control subjects we were unable to detect a significant difference in the expression of collagenase type I and IV in Crohn's disease; in contrast, we observed a significant increase in the rate of expression for the collagenases in ulcerative colitis as compared to controls or biopsies from patients with Crohn's disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Altered glycosylation of integrin adhesion molecules in colorectal cancer cells and decreased adhesion to the extracellular matrix.

The integrin mediated interactions between tumour cells and the surrounding extracellular matrix are thought to play crucial parts in the complex process of invasion and metastasis. It has been previously shown that the expression of integrins is differently diminished in a chain-specific manner in human colorectal cancer. To further characterise the integrins still expressed in colorectal carcinomas, immunoblots with monoclonal antibodies against the beta 1 integrin subunit have been performed. In isolated cell membranes of colorectal cancers a second smaller beta 1 chain (105 kD non-reduced) was found as well as the mature beta 1 chain (116 kD non-reduced) present in normal mucosa of the colon. This smaller beta 1 chain comigrates with the diminished glycosylated precursor form of the beta 1 chain. The role of N-glycosylation for the function and expression of integrins in vitro was therefore investigated, with deoxymannojirimycin (DMJ) and deoxynojirimycin (DNJ) as specific inhibitors of N-glycan processing. Pretreatment of human colon adenocarcinoma derived HT-29 cells with DMJ resulted in an expression of the 105 kD beta 1 precursor chain and of smaller forms of the alpha 1, alpha 3, alpha 6, and alpha v integrin subunits in a time and dose dependent manner. HT-29 cells treated with DMJ adhered poorly to laminin (8% of untreated controls), collagen type IV (40%), and fibronectin (35%). Pretreatment of the cells with DNJ did not alter the molecular weight of the integrin chains expressed and reduced HT-29 adhesion to laminin and fibronectin only to 68% and 49% respectively. Adhesion to collagen type IV was increased to 124% by DNJ. These results show that N-glycan processing is essential for the function and expression of integrins in human colorectal cancer cells. An altered glycosylation of these adhesion receptors may contribute to a more invasive or metastatic phenotype in colorectal cancer.

Adenocarcinoma↗
PubMed1992

[Colorectal carcinoma--current pathogenetic concepts. Significance of cell-matrix interaction for invasive growth and metastasis].

Altered expression of certain cell-matrix receptors has been found to be specific for malignant, transformed epithelial cells in the large intestine. An attractive hypothesis, therefore, is that invasion and metastasis result from characteristic changes of these cell adhesion molecules. In animal models, it was possible to reduce the frequency of tumor invasion and metastasis and to achieve longer survival by modifications of cell membrane binding components on malignant cells. An increasing understanding of the role of receptor-mediated epithelium-matrix interactions in malignancy facilitates the development of new therapeutic concepts.

Animals↗
PubMed1992

Cellular localization of procollagen gene transcripts in inflammatory bowel diseases.

The cellular localization of procollagen types I, III, IV, and V gene transcripts was determined in tissues from 12 patients with either Crohn's disease (CD) or ulcerative colitis (UC) and nine controls by in situ hybridization with 35S-labeled RNA probes. In CD, the signal intensity and number of labeled cells were significantly increased, particularly in deeper intestinal layers. In contrast, the labeled cells in UC were concentrated in the subepithelial intestinal layers, with an overexpression of procollagen III RNA transcripts. Immunohistological stainings for procollagen types I, III, and IV showed a weaker staining in UC than in CD, indicating that increased transcript levels in UC are unrelated to the enhanced collagen protein deposition, although the increase of procollagen messenger RNA levels correlated with the density of the inflammatory infiltrate. It was concluded that both CD and UC show highly increased procollagen RNA transcript levels but differ in collagen deposition. Thus, different posttranscriptional or posttranslational regulatory mechanisms, such as collagen degradation, may account for the observed differences.

Adult↗
PubMed1992

Increased collagen type III synthesis by fibroblasts isolated from strictures of patients with Crohn's disease.

Increased type III collagen deposition in all layers of the intestinal tract, including the lamina propria, is a common feature of strictures in Crohn's disease. In the present study, it was found that in comparison with fibroblasts from normal or nonstrictured but inflamed intestinal lamina propria, the fibroblasts isolated from strictures of patients with Crohn's disease produce significantly more collagen, especially collagen type III. Transforming growth factor beta 1 (TGF-beta 1) significantly increased collagen type III synthesis in intestinal lamina propria fibroblasts isolated from all patients. The effect of TGF-beta 1 on type III collagen synthesis in fibroblasts from strictures in Crohn's disease was significantly higher than that in fibroblasts from inflamed specimens of the same patients. In contrast, platelet-derived growth factor decreased collagen type III synthesis in lamina propria fibroblasts derived from strictures compared with fibroblasts from nonstrictured but inflamed tissue. These findings indicate that fibroblasts in the lamina propria of patients with Crohn's disease have a different reactivity towards cytokines. On the basis of increased type III collagen deposition in intestinal strictures of Crohn's disease by using cell adhesion and cell proliferation assays, it was shown that collagen type III stimulated adhesion and proliferation of lamina propria fibroblasts. The current data provide evidence that the different reactivity of mesenchymal cells to cytokines in terms of synthesizing type III collagen fibrils, which is a major component of collagen fibrils, may play an important role in the pathogenesis of fibrosis and stricture formation in chronic inflammatory bowel diseases.

Adult↗
PubMed1992

Laminin binding in membranes of a rat pancreatic acinar cell line are targets for glucocorticoids.

The adhesive properties of tumor cells to basement membranes are known to play a crucial role in the complex process of tumor invasion and metastasis. Therefore, the interaction between the rat pancreatic acinar cell line AR42J and various extracellular matrix components along the route of differentiation induced by glucocorticoids was investigated. AR42J cells displayed a significantly higher affinity to laminin than to type IV collagen and fibronectin. Flow cytometric analysis showed expression of the 67-kilodalton laminin receptor and the integrin VLA-6 as potential laminin binding proteins in AR42J cells. Cell adhesion inhibition studies revealed that binding of undifferentiated AR42J cells to laminin was mediated predominantly by the 67-kilodalton laminin receptor. Dexamethasone pretreatment, which results in a more differentiated phenotype of AR42J cells, reduced the adhesion to laminin. In contrast to undifferentiated cells, interaction of differentiated AR42J cells to laminin was mediated by VLA-6. Dexamethasone-induced differentiation of pancreatic AR42J cells was paralleled by a decreased expression of 67-kilodalton laminin receptors, most likely because of a downregulation of the steady-state concentration of 67-kilodalton laminin receptor messenger RNA induced by dexamethasone. The hormonal modulation of cell matrix interactions opens interesting perspectives to the potential regulation of infiltrative growth and metastasis in pancreatic cancer.

Animals↗
PubMed1992

Diminished expression of integrin adhesion molecules on human colonic epithelial cells during the benign to malign tumour transformation.

Integrins are transmembrane molecules that mediate cell-cell and cell-substratum adhesion. Because alterations in the adhesive properties of tumour cells are thought to influence tumour cell invasion, the expression of integrin alpha and beta chains in 19 human colorectal carcinomas, eight adenomas, and eight normal colon tissues was examined immunohistochemically using an indirect immunofluorescent technique. Normal colonic epithelial cells were found to express the integrin alpha 3, alpha 5, alpha 6, beta 1, and beta 4 chains, whereas the alpha 2 chain was expressed only on epithelial cells lining the base of the crypts and was absent from cells lining the mouth of the crypts or the surface epithelium. No epithelial staining of the alpha 1, alpha 4, beta 2, and beta 3 chains was observed. A progressive reduction of all normally expressed alpha and beta chains was associated with increasing neoplastic transformation. The expression of the alpha 3 and alpha 5 chains was already noticeably reduced in adenomas, and was completely absent in most colonic carcinomas. In contrast, alpha 6, beta 1, and beta 4 expression was maintained in adenomas, whereas the transformation from benign to malignant neoplasms associated with infiltrative growth was characterised by diminished or lost expression of alpha 6, beta 1, and beta 4 chains. Thus, the decreased expression of integrins in human colon carcinomas may contribute to the altered adhesion and migration properties of these tumour cells.

Adenocarcinoma↗
PubMed1991

Identification of different laminin binding proteins in basolateral cell membranes of human colorectal carcinomas and normal colonic mucosa.

The adhesive properties of tumour cells to laminin, the major glycoprotein of basement membranes, play a crucial part in the complex process of tumour invasion and metastasis. We therefore investigated the expression of laminin binding proteins in isolated basolateral cell membranes of human colorectal carcinomas and the adjacent normal colonic mucosa. Cell membrane binding assays and immunoblotting experiments showed appreciable quantitative and qualitative differences in the expression of these proteins in neoplastic and normal tissue. Epithelial basolateral cell membranes of colorectal carcinomas bound five to eight times more radioactive labelled laminin than basolateral cell membranes of the adjacent normal colonic epithelium. The expression of laminin binding proteins with Mr 66,000-69,000 daltons corresponding to the so called 'Mr 67,000 dalton laminin receptor' was three to four times higher in colorectal carcinomas than in normal colonic epithelium. In addition, laminin binding proteins with higher molecular weights, which may be related to the family of integrins, were also increased in colorectal carcinomas. In particular, laminin binding proteins with Mr 180,000 daltons were exclusively expressed on neoplastic epithelial cells of human colorectal carcinomas. Our data suggest that certain classes of laminin binding proteins may be selectively expressed on colonic tumour cells, leading to an increased capacity for migration, invasion, and metastasis.

Carrier Proteins↗