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Grunberg W.,University Utrecht | Dobbelaar P.,University Utrecht | Breves G.,Physiologisches Institute
British Journal of Nutrition

Hypophosphataemia is frequently encountered in dairy cows during early lactation. Although supplementation of P is generally recommended, controversy exists over the suitability of oral P supplementation in animals with decreased or absent rumen motility. Since the effects of transruminal P absorption and the reticular groove reflex on the absorption kinetics of P are not well understood, it is unclear in how far treatment efficacy of oral P supplementation is affected by decreased rumen motility. Phosphate absorption was studied in six phosphate-depleted dairy cows fitted with rumen cannulas and treated with test solutions containing either NaH2PO4 or CaHPO4 with acetaminophen. Each animal was treated orally, intraruminally and intra-abomasally in randomised order. Absorption kinetics of P were studied and compared with the absorption kinetics of acetaminophen, a marker substance only absorbed from the small intestine. Intra-abomasal treatment with NaH2PO4 resulted in the most rapid and highest peaks in plasma inorganic P (Pi) concentration. Oral and intraruminal administration of NaH2PO4 resulted in similar increases in plasma Pi concentration from 4 to 7Â h in both groups. Treatment with NaH2PO4 caused more pronounced peaks in plasma Pi concentration compared with CaHPO4. Neither transruminal P absorption nor the reticular groove reflex affected P absorption kinetics as determined by comparing plasma concentration-time curves of P and acetaminophen after administration of 1Â m-phosphate salt solutions. It is concluded that oral treatment with NaH2PO4 but not CaHPO4 is effective in supplementing P in hypophosphataemic cows with adequate rumen motility. Decreased rumen motility is likely to hamper the efficacy of oral phosphate treatment. Copyright © The Authors 2013. Source

Leonhard-Marek S.,Physiologisches Institute
Archiv fur Lebensmittelhygiene

Stress as a physiological response to a changed environment serves as a short-term defence mechanism. In the long term, however, stress can severely impair health and production parameters. Within the udder, stress has an influence on all functions from milk synthesis to the processes of milk secretion and milk ejection. In addition, stress acts upon the defence mechanisms of the mammary gland. © M. & H. Schaper GmbH & Co. Source

Wenzel S.,Justus Liebig University | Wenzel S.,Physiologisches Institute | Henning K.,Justus Liebig University | Habbig A.,Justus Liebig University | And 5 more authors.
Basic Research in Cardiology

TGF-β1 plays an important role in cardiac fibrosis, apoptosis, induction of hypertrophy and contractile dysfunction. This study investigates whether TGF-β1 plays a role in laminin receptor 37/67 (37/67 LR)-dependent regulation of cardiac performance. Therefore, isolated adult cardiomyocytes were stimulated with TGF-β1, the expression of the 37/67 LR was determined and cell shortening was investigated on cells attached to a non-specific, serum-based attachment substrate or to specific, laminin-coated dishes. The role of the MAP kinases in TGF-β1-dependent induction of the 37/67 LR was examined by addition of PD98059, SB202190 and SP600125. Finally, the expression of receptor mRNA was investigated in transgenic mice constitutively over-expressing TGF-β1 and the relationship to distress score and lung wet weight-to-body weight was analysed. TGF-β1 induced a significant increase of the 37/67 LR mRNA and protein expression. The cytokine induced p38 MAP kinase and JNK, but not ERK. Inhibition of either p38 MAP kinase or JNK attenuated the TGF-β1-dependent increase in 37/67 LR expression. TGF-β1 induced a loss of cell shortening in cells attached to a non-specific substrate, but not in cells on a pre-coated laminin matrix. Inhibition of JNK attenuated the protective effect of laminin receptor up-regulation on cardiac performance. Inhibition of p38 MAP kinase attenuated the depressive effect of TGF-β1 on basal cell shortening. In transgenic mice over-expressing TGF-β1 a strong induction of laminin receptor expression attenuated the severeness of the mice' symptoms. This study shows a new and protective role of TGF-β1-dependent up-regulation of the 37/67 LR in cardiomyocytes in cardiac remodelling with increased laminin expression. © 2010 Springer-Verlag. Source

Schwab A.,University of Munster | Nechyporuk-Zloy V.,University of Glasgow | Gassner B.,Physiologisches Institute | Schulz C.,Ludwig Maximilians University of Munich | And 4 more authors.
Journal of Cellular Physiology

Calcium-sensitive potassium channels (K Ca3.1) are expressed in virtually all migrating cells. Their activity is required for optimal cell migration so that their blockade leads to slowing down. K Ca3.1 channels must be inserted into the plasma membrane in order to elicit their physiological function. However, the plasma membrane of migrating cells is subject to rapid recycling by means of endo- and exocytosis. Here, we focussed on the endocytic internalization and the intracellular transport of the human isoform hK Ca3.1. A hK Ca3.1 channel construct with an HA-tag in the extracellularly located S3-S4 linker was transfected into migrating transformed renal epithelial MDCK-F cells. Channel internalization was visualized and quantified with immunofluorescence and a cell-based ELISA. Movement of hK Ca3.1 channel containing vesicles as well as migration of MDCK-F cells were monitored by means of time lapse video microscopy. hK Ca3.1 channels are endocytosed during migration. Most of the hK Ca3.1 channel containing vesicles are moving at a speed of up to 2μm/sec in a microtubule-dependent manner towards the front of MDCK-F cells. Our experiments indicate that endocytosis of hK Ca3.1 channels is clathrin-dependent since they colocalize with clathrin adaptor proteins and since it is impaired when a C-terminal dileucine motif is mutated. The C-terminal dileucine motif is also important for the subcellular localization of hK Ca3.1 channels in migrating cells. Mutated channels are no longer concentrated at the leading edge. We therefore propose that recycling of hK Ca3.1 channels contributes to their characteristic subcellular distribution in migrating cells. © 2011 Wiley Periodicals, Inc. Source

Fluck K.,University of Duisburg - Essen | Fluck K.,Physiologisches Institute | Breves G.,Physiologisches Institute | Fandrey J.,University of Duisburg - Essen | Winning S.,University of Duisburg - Essen
Mucosal Immunology

Dendritic cells (DCs) serve as a bridge between innate and adaptive immunity and help to maintain intestinal homeostasis. Inflammatory bowel disease (IBD) is associated with dysregulation of the mucosal immune response. The concomitant hypoxic inflammation in IBD will activate the transcription factor hypoxia-inducible factor-1 (HIF-1) to also drive gene expression in DCs. Recent studies have described a protective role for epithelial HIF-1 in mouse models of IBD. We investigated the role of HIF-1 in DC function in a dextran sodium sulfate (DSS)-induced model of murine colitis. Wild-type and dendritic cell-specific HIF-1α knockout mice were treated with 3% DSS for 7 days. Knockout of HIF-1α in DCs led to a significantly larger loss of body weight in mice with DSS-induced colitis than in control mice. Knockout mice exhibited more severe intestinal inflammation with increased levels of proinflammatory cytokines and enhanced production of mucin. Induction of regulatory T cells (Tregs) was impaired, and the number of forkhead box P3 (Foxp3) Tregs was diminished by dendritic HIF-1α knockout. Our findings demonstrate that in DCs HIF-1α is necessary for the induction of sufficient numbers of Tregs to control intestinal inflammation. Source

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