排序方式: 共有76条查询结果,搜索用时 31 毫秒
1.
Roeland Van Wijk Marij Welters Jan E. M. Souren Hans Ovelgonne Fred A. C. Wiegant 《Journal of cellular physiology》1993,155(2):265-272
In this work, we demonstrate that a nonlethal dose of arsenite administered to quiescent C3H10T1/2 fibroblasts can enhance the mitogenic effect of suboptimal concentrations of serum. The mitogenic effect was dependent on the serum concentration and on the time interval between the administration of arsenite and that of serum. This suggests that mitogen sensitivity changes in time after arsenite treatment. It is shown that the concentrations of arsenite that enhance the mitogenic effect of serum also increase the mRNA levels of c-fos, HSP68, and HSP84 and induce the specific synthesis of Heat Shock Proteins (HSPs). The physiological significance of this phenomenon is most likely to counteract the long-term toxic effect of arsenite by early induction of compensation for cell loss. © 1993 Wiley-Liss, Inc. 相似文献
2.
3.
Deepak Jain Gesine Weber Daniel Eberhard Amir E. Mehana Jan Eglinger Alena Welters Barbara Bartosinska Kay Jeruschke Jürgen Weiss Günter P?th Hiroyoshi Ariga Jochen Seufert Eckhard Lammert 《PloS one》2015,10(9)
A hallmark feature of type 1 and type 2 diabetes mellitus is the progressive dysfunction and loss of insulin-producing pancreatic beta cells, and inflammatory cytokines are known to trigger beta cell death. Here we asked whether the anti-oxidant protein DJ-1 encoded by the Parkinson’s disease gene PARK7 protects islet cells from cytokine- and streptozotocin-mediated cell death. Wild type and DJ-1 knockout mice (KO) were treated with multiple low doses of streptozotocin (MLDS) to induce inflammatory beta cell stress and cell death. Subsequently, glucose tolerance tests were performed, and plasma insulin as well as fasting and random blood glucose concentrations were monitored. Mitochondrial morphology and number of insulin granules were quantified in beta cells. Moreover, islet cell damage was determined in vitro after streptozotocin and cytokine treatment of isolated wild type and DJ-1 KO islets using calcein AM/ethidium homodimer-1 staining and TUNEL staining. Compared to wild type mice, DJ-1 KO mice became diabetic following MLDS treatment. Insulin concentrations were substantially reduced, and fasting blood glucose concentrations were significantly higher in MLDS-treated DJ-1 KO mice compared to equally treated wild type mice. Rates of beta cell apoptosis upon MLDS treatment were twofold higher in DJ-1 KO mice compared to wild type mice, and in vitro inflammatory cytokines led to twice as much beta cell death in pancreatic islets from DJ-1 KO mice versus those of wild type mice. In conclusion, this study identified the anti-oxidant protein DJ-1 as being capable of protecting pancreatic islet cells from cell death induced by an inflammatory and cytotoxic setting. 相似文献
4.
Mühling J Burchert D Langefeld TW Matejec R Harbach H Engel J Wolff M Welters ID Fuchs M Menges T Krüll M Hempelmann G 《Amino acids》2007,33(3):511-524
Summary. We examined the effects of DON [glutamine-analogue and inhibitor of glutamine-requiring enzymes], alanyl-glutamine (regarding
its role in neutrophil immunonutrition) and alanyl-glutamine combined with L-NAME, SNAP, DON, β-alanine and DFMO on neutrophil
amino and α-keto acid concentrations or important neutrophil immune functions in order to establish whether an inhibitor of
•NO-synthase [L-NAME], an •NO donor [SNAP], an analogue of taurine and a taurine transport antagonist [β-alanine], an inhibitor
of ornithine-decarboxylase [DFMO] as well as DON could influence any of the alanyl-glutamine-induced effects. In summary,
irrespective of which pharmacological, metabolism-inhibiting or receptor-mediated mechanisms were involved, our results showed
that impairment of granulocytic glutamine uptake, modulation of intracellular glutamine metabolisation and/or de novo synthesis
as well as a blockade of important glutamine-dependent metabolic processes may led to significant modifications of physiological
and immunological functions of the affected cells. 相似文献
5.
Goumon Y Angelone T Schoentgen F Chasserot-Golaz S Almas B Fukami MM Langley K Welters ID Tota B Aunis D Metz-Boutigue MH 《The Journal of biological chemistry》2004,279(13):13054-13064
Phosphatidylethanolamine-binding protein (PEBP), alternatively named Raf-1 kinase inhibitor protein, is the precursor of the hippocampal cholinergic neurostimulating peptide (HCNP) corresponding to its natural N-terminal fragment, previously described to be released by hippocampal neurons. PEBP is a soluble cytoplasmic protein, also associated with plasma and reticulum membranes of numerous cell types. In the present report, using biochemistry and cell biology techniques, we report for the first time the presence of PEBP in bovine chromaffin cell, a well described secretion model. We have examined its presence at the subcellular level and characterized this protein on both secretory granule membranes and intragranular matrix. In addition, its presence in bovine chromaffin cell and platelet exocytotic medium, as well as in serum, was reported showing that it is secreted. Like many other proteins that lack signal sequence, PEBP may be secreted through non-classic signal secretory mechanisms, which could be due to interactions with granule membrane lipids and lipid rafts. By two-dimensional liquid chromatography-tandem mass spectrometry, HCNP was detected among the intragranular matrix components. The observation that PEBP and HCNP were secreted with catecholamines into the circulation prompted us to investigate endocrine effects of this peptide on cardiovascular system. By using as bioassay an isolated and perfused frog (Rana esculenta) heart preparation, we show here that HCNP acts on the cardiac mechanical performance exerting a negative inotropism and counteracting the adrenergic stimulation of isoproterenol. All together, these data suggest that PEBP and HCNP might be considered as new endocrine factors involved in cardiac physiology. 相似文献
6.
Mühling J Engel J Halabi M Müller M Fuchs M Krüll M Harbach H Langefeld TW Wolff M Matejec R Welters ID Menges T Hempelmann G 《Amino acids》2006,31(1):11-26
Summary. We have examined the effects of Nω-nitro-L-arginine-methylester-hydrochloride [L-NAME; inhibitor of nitric oxide synthase], S-nitroso-N-acetyl-penicillamine
[SNAP; nitric oxide donor], α-difluoro-methyl-ornithine [DFMO; inhibitor of ornithine decarboxylase] arginine or ornithine
as well as the combination of arginine or ornithine with L-NAME, SNAP or DFMO on intracellular free amino- and α-keto acid
profiles and the immune function markers superoxide anion and hydrogen peroxide generation as well as released myeloperoxidase
activity in neutrophils (PMN). Although the underlying mechanisms still remain unclear, we believe from our results that nitric
oxide as well as polyamine-dependent pathways are involved in the signal transmission of free radical molecule, beneficial
nutritional therapy or maleficient pharmacological stress-induced alterations in PMN nutrient composition. Relevant changes
in intragranulocyte free amino- and α-keto acid homeostasis and metabolism, especially, may be one of the determinants in
PMN nutrition that positively or negatively influences and modulate neutrophil host defence capability and immunocompetence. 相似文献
7.
Mühling J Nickolaus KA Matejec R Langefeld TW Harbach H Engel J Wolff M Weismüller K Fuchs M Welters ID Krüll M Heidt MC Hempelmann G 《Amino acids》2008,34(2):257-270
We examined the effects of beta-alanine (taurine analogue and taurine transport antagonist), taurine (regarding its role in neutrophil (PMN) immunonutrition) and taurine combined either with L-NAME (inhibitor of *NO-synthase), SNAP (*NO donor), DON (glutamine-analogue and inhibitor of glutamine-requiring enzymes), DFMO (inhibitor of ornithine-decarboxylase) and beta-alanine on neutrophil amino- and alpha-keto acid profiles or important PMN immune functions in order to establish whether taurine transport-, nitric oxide-, glutamine- or ornithine-dependent mechanisms are involved in any of the taurine-induced effects. According to the present findings, the taurine-mediated effect appears to be based primarily on a modulation of important transmembraneous transport mechanisms and only secondarily on directly or indirectly induced modifications in intragranulocytic amino- and alpha-keto acid homoeostasis or metabolism. Although a direct relation to the parallel observed immunological modifications can only be presumed, these results show very clearly that compositional modifications in the free intragranulocytic amino- and alpha keto-acid pools coinciding with changes in intragranulocytic taurine levels are relevant metabolic determinants that can significantly influence the magnitude and quality of the granulocytic immune response. 相似文献
8.
9.