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190 results on '"Bachem, M."'

11. Frakturheilung - Callusmodulation I - Standortbestimmung

Author

Claes, L., primary, Wolf, S., additional, Janousek, A., additional, Pfeil, J., additional, Schmelz, A., additional, Bachem, M., additional, Suger, G., additional, Kinzl, L., additional, Kröpfl, A., additional, Berger, U., additional, Redl, H., additional, Schlag, G., additional, and Hertz, H., additional

Published
2000
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12. Varia

Author

Calvete, J. J., Schäfer, W., Henschen, A., Gonzalez-Rodriguez, J., Sichtermann, W., Wenclawiak, B., Schipke, J., Benninghoven, A., Meese, C. O., Specht, D., Fischer, P., Hübner, D., Fischer, G., Ströhl, D., Kleinpeter, E., Hartrodt, B., Brandt, W., Gauglitz, G., Walz, R., Wälder, H., Lipinski, J., Stan, H. -J., Waidmann, E., Hilpert, K., Stoeppler, M., Welz, Bernhard, Sperling, Michael, Fang, Zhaolun, Fink, E., Hehlein-Fink, C., Nast-Kolb, D., Jochum, M., Ohlsson, K., Dietze, S., Auerswald, E. A., Fritz, H., Pfeilschifter, Josef, Leighton, Jonathan, Pignat, Werner, Märki, Fritz, Vosbeck, Klaus, Bachem, M. G., Meyer, D. H., Gressner, A. M., Ratge, D., Steegmüller, U., Wisser, H., Dargel, R., Schlag, B., Winkler, L., Müller, H., Oswald, B., Schumann, G., Petersen, D., Büttner, J., and Maurer, Hans H.

Published
1990
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20. TGFbeta and the extracellular matrix in pancreatitis

Author

Muller-Pillasch F, Menke A, Yamaguchi H, Hp, Elsasser, Bachem M, Adler G, and Thomas Gress

Subjects
Disease Models, Animal, Mice, Pancreatitis, Transforming Growth Factor beta, Acute Disease, Animals, Humans, Regeneration, Extracellular Matrix, Rats
Abstract

Regeneration from cerulein-induced pancreatitis is accompanied by a transient synthesis and deposition of extracellular matrix components in the rat pancreas. To study the involvement of transforming growth factor beta1 (TGFbeta1), one of the most potent modulators of the extracellular matrix, in the process of pancreatic regeneration we examined the expression of this gene on the transcript and protein level in pancreata of rats sacrificed 0 hours, 24 hours, 2, 3, 5, 7 days after a 12 hour infusion of maximal doses of cerulein (10 microg kg(-1) h(-1)). TGFbeta1 protein increased twofold after 24 hours and 48 hours and returned to control values 7 days after induction of pancreatitis, while TGFbeta1-mRNA reached maximal values (3-fold over controls) after 2 days. The largest amount of TGFbeta1 mRNA was found in pancreatic acinar cells and in stromal cells. To verify the functional implication of TGFbeta overexpression in regulating extracellular matrix remodeling during regeneration from acute pancreatitis, rats were treated with 3 injections of neutralizing antibody against TGFbeta1 given 30 min before, and 24 hours and 48 hours after the start of infusion. In rats treated with maximal doses of cerulein and TGFbeta antibodies, pancreatic hydroxyproline content and expression of collagens I and III and of TGFbeta1 were significantly reduced. These results provide evidence that transforming growth factor beta1 among other cytokines is involved in the regulation of extracellular matrix remodeling in the rat pancreas during regeneration from cerulein-induced acute pancreatitis. In addition, there is evidence in the literature that application of recombinant TGFbeta after recurrent episodes of acute cerulein-induced pancreatitis promotes pancreatic fibrosis (3). Thus, TGFbeta is a regulator of extracellular matrix remodeling in the pancreas, and may be an important promoting factor in the pathogenesis of chronic pancreatitis. This hypothesis is supported by data in the literature showing enhanced TGFbeta expression in human chronic pancreatitis (2) and development of fibrosis and inflammation in pancreata of transgenic mice overexpressing TGFbeta1 (3).

Published
1999

30. Induktion und Regulation der Hämoxygenase-1 in humanen Hepatozyten

Author

Nüssler, Andreas, Luft, Friedrich C., Bachem, M. G., Müller, Eda, Nüssler, Andreas, Luft, Friedrich C., Bachem, M. G., and Müller, Eda

Abstract

Der nach Leberoperation und -transplantation auftretende Ischämie-/ Reperfusionsschaden (I/R) und die konsekutive Inflammation des Lebergewebes stellen ein bedeutendes klinisches Problem dar. In der vorliegenden Arbeit wurden Einflüsse der warmen und kalten Ischämie (100% N2 bei 37°C bzw. 4°C) sowie der Exposition inflammatorischer Zytokine und Endotoxin (IL-1beta, 10 U/ml; IFN-gamma, 100 U/ml; TNF-alpha, 500 U/ml; LPS, 5 µg/ml) auf die Expression der Hämoxygenase-1 (HO- 1) mRNA und seines Proteins, einem Vertreter der Hitze-Schock-Proteine mit potentiell antioxidativer Wirkung, in humanen Hepatozytenprimärkulturen untersucht. Warme und kalte Ischämie stimulierten die HO-1 mRNA Expression in humanen Hepatozyten nach 0,5 bis 1h. Das HO-1 Protein wurde über 0,5-6h maximal exprimiert. Der Zellschaden, gemessen an der AST und LDH Freisetzung unter ischämischen Bedingungen wurde insbesondere nach 24 h beobachtet. Nach Zytokinexposition wurde die höchste Expressionsrate der mRNA durch IFN-gamma hervorgerufen, gefolgt von TNF-alpha, LPS und IL-1beta. Jedes einzelne Zytokin stimulierte die HO-1 mRNA Expression nach 0,5 h, erreichte ein Maximum nach 3 h und fiel nach 6 h ab. Nach Stimulation mit einem Zytokinmix (CM; IFN-gamma, TNF-alpha, IL-1beta, LPS) trat ein Maximum der HO-1 mRNA Expression erst nach 6 h ein, wobei ein signifikanter Zellschaden nach 12 h beobachtet wurde. Die HO-1 mRNA und Proteinexpression war nach Exposition von 6 h des Sauerstoffperoxides (H2O2, 200- 1000 µM) erhöht. Die HO-1 mRNA und Proteinexpression war nach S- nitrosoacetylpenicillamin (0.5 mM) Exposition, einem NO Donator, für 3-12 h verstärkt. Nach Cobalt-protoporphyrin (CoPP, 1µM) Exposition, einem potenten HO-1 Induktor, wurde eine erhöhte mRNA- und Proteinexpression beobachtet. Dass CoPP die HO-1 mRNA- und Proteinneusynthese induziert, konnte durch die selektive Blockade mit Actinomycin D und Cycloheximide bewiesen werden. Die Neusynthese konnte ebenfalls unter warmer und kalter Ischämie geze, Hepatic injury induced by ischemia/ reperfusion (I/R) and inflammation following surgeries or transplantations creates important clinical problems. In this study, the effect of inflammatory conditions such as cytokine/ endotoxin exposure (IL-1beta, IFN-gamma, TNF-alpha, LPS), warm and cold ischemia on HO-1 mRNA and protein, a member of heat shock proteins, was investigated. It was observed that IFN-gamma caused the highest HO-1 mRNA expression, followed by TNF-alpha, LPS and IL- 1beta. Each stimuli increased HO-1 mRNA expression after 0.5 h, peaked at 3 h and decreased after 6 h. Highest HO-1 protein expression was observed after 0.5 to 1 h of stimulation with IFN-gamma, which was followed by LPS, TNF-alpha and IL-1beta. The peak of HO-1 expression using all four stimuli (CM) was after 6 h. CM caused a significant increase in LDH and AST after 12 h. Warm and cold ischemia stimulated HO-1 mRNA expression in human hepatocytes at 0.5-1 h. HO-1 protein expression had its maximum between 0.5-6 h. Cellular damage measured as the release of LDH and AST was significant after 24 h. Mimicking oxydative stress, hepatocytes were exposed to 200-1000 µM H2O2 for 6 h which also showed an increased HO-1 mRNA and protein expression. HO-1 mRNA and protein expression revealed an increase after SNAP exposure at 3-12 h. Results with CoPP (10 µM), a potent inducer of HO- 1, displayed an increase in HO-1 mRNA and protein expression. It was proved, that CoPP induced new synthesis of mRNA and protein by its blocking agents such as actinomycin D and cycloheximide, respectively. Hemin (10 µM), another inducer of HO-1, triggered HO-1 mRNA expression after 3 h and protein expression after 6 h. The HO-1 enzyme activity was measured by bilirubin production after exposure to CM, as well as warm and cold ischemia. The highest enzyme activity was found after warm ischemia, followed by cold ischemia, CM and then by the control group. Fe2+ content of the cells, used as another method to judge HO-1 act

Published
2002

34. Islet Stellate Cells Isolated from Fibrotic Islet of Goto-Kakizaki Rats Affect Biological Behavior of Beta-Cell.

Author

Li, Feng-Fei, Chen, Bi-Jun, Li, Wei, Li, Ling, Zha, Min, Zhou, S., Bachem, M. G., and Sun, Zi-Lin

Subjects
KUPFFER cells, LABORATORY rats, CELL proliferation, TREATMENT of diabetes, GENETICS of diabetes, GENE expression
Abstract

We previously isolated islet stellate cells (ISCs) from healthy Wistar rat islets. In the present study, we isolated “already primed by diabetic environment” ISCs from islets of Goto-Kakizaki rats, determined the gene profile of these cells, and assessed the effects of these ISCs on beta-cell function and survival. We detected gene expression of ISCs by digital gene expression. INS-1 cell proliferation, apoptosis, and insulin production were measured after being treated with ISCs supernatant (SN). We observed the similar expression pattern of ISCs and PSCs, but 1067 differentially expressed genes. Insulin production in INS-1 cells cultured with ISC-SN was significantly reduced. The 5-ethynyl-2′-deoxyuridine-positive INS-1 cells treated with ISC-SN were decreased. Propidium iodide- (PI-) positive INS-1 cells were 2.6-fold higher than those in control groups. Caspase-3 activity was increased. In conclusion, ISCs presented in fibrotic islet of GK rats might be special PSCs, which impaired beta-cell function and proliferation and increased beta-cell apoptosis. [ABSTRACT FROM AUTHOR]

Published
2015
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45. Pancreatic stellate cells promote hapto-migration of cancer cells through collagen I-mediated signalling pathway.

Author

Lu, J, Zhou, S, Siech, M, Habisch, H, Seufferlein, T, and Bachem, M G

Abstract

Background: Pancreatic stellate cells (PSCs) promote metastasis as well as local growth of pancreatic cancer. However, the factors mediating the effect of PSCs on pancreatic cancer cells have not been clearly identified.Methods: We used a modified Boyden chamber assay as an in vitro model to investigate the role of PSCs in migration of Panc1 and UlaPaCa cells and to identify the underlying mechanisms.Results: PSC supernatant (PSC-SN) dose-dependently induced the trans-migration of Panc1 and UlaPaCa cells, mainly via haptokinesis and haptotaxis, respectively. In contrast to poly-L-lysine or fibronectin, collagen I resembled PSC-SN with respect to its effect on cancer cell behaviours, including polarised morphology, facilitated adhesion, accelerated motility and stimulated trans-migration. Blocking antibodies against integrin α2/β1 subunits significantly attenuated PSC-SN- or collagen I-promoted cell trans-migration and adhesion. Moreover, both PSC-SN and collagen I induced the formation of F-actin and focal adhesions in cells, which was consistent with the constantly enhanced phosphorylation of focal adhesion kinase (FAK, Tyr397). Inhibition of FAK function by an inhibitor or small interference RNAs significantly diminished the effect of PSC-SN or collagen I on haptotaxis/haptokinesis of pancreatic cancer cells.Conclusion: Collagen I is the major mediator for PSC-SN-induced haptokinesis of Panc1 and haptotaxis of UlaPaCa by activating FAK signalling via binding to integrin α2β1. [ABSTRACT FROM AUTHOR]

Published
2014
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49. Inhibition of endogenous SPARC enhances pancreatic cancer cell growth: modulation by FGFR1-III isoform expression.

Author

Chen, G., Tian, X., Liu, Z., Zhou, S., Schmidt, B., Henne-Bruns, D., Bachem, M., and Kornmann, M.

Subjects
CYSTEINE proteinases, TUMOR suppressor genes, ADENOCARCINOMA, PANCREATECTOMY, XENOGRAFTS, FIBROBLAST growth factors, GENE expression, CELL division, CELL lines, CELL physiology, CELL motility, CELL receptors, COMPARATIVE studies, CULTURE media (Biology), GENES, GLYCOPROTEINS, IMIDAZOLES, RESEARCH methodology, MEDICAL cooperation, PANCREATIC tumors, PROTEINS, PYRIDINE, RECOMBINANT proteins, RESEARCH, TRANSFERASES, PHENOTYPES, EVALUATION research, DUCTAL carcinoma, CHEMICAL inhibitors, PHARMACODYNAMICS
Abstract

Background: Secreted protein acidic and rich in cysteine (SPARC) is a multi-faceted protein-modulating cell-cell and cell-matrix interactions. In cancer, SPARC can be not only associated with a highly aggressive phenotype, but also acts as a tumour suppressor. The aim of this study was to characterise the function of SPARC and its modulation by fibroblast growth factor receptor (FGFR) 1 isoforms in pancreatic ductal adenocarcinoma (PDAC).Methods and Results: Exogenous SPARC inhibited growth, movement, and migration. ShRNA inhibition of endogenous SPARC in ASPC-1 and PANC-1 cells resulted in increased anchorage-dependent and -independent growth, transwell migration, and xenograft growth as well as increased mitogenic efficacy of fibroblast growth factor (FGF) 1 and FGF2. Endogenous SPARC expression in PANC-1 cells was increased in FGFR1-IIIb over-expressing cells, but decreased in FGFR1-IIIc over-expressing cells. The up-regulation of endogenous SPARC was abrogated by the p38-mitogen-activated protein kinase inhibitor SB203580. SPARC was detectable in conditioned medium of pancreatic stellate cells (PSCs), but not PDAC cells. Conditioned medium of PDAC cells reduced endogenous SPARC expression of PSCs.Conclusion: Endogenous SPARC inhibits the malignant phenotype of PDAC cells and may, therefore, act as a tumour suppressor in PDAC. Endogenous SPARC expression can be modulated by FGFR1-III isoform expression. In addition, PDAC cells may inhibit endogenous SPARC expression in surrounding PSCs by paracrine actions. [ABSTRACT FROM AUTHOR]

Published
2010
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