Brigitte Rausch
Hannover Medical School
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Publication
Featured researches published by Brigitte Rausch.
Journal of Clinical Investigation | 2009
Anurag Singh; Brigitte Riederer; Anja Krabbenhöft; Brigitte Rausch; Janina Bonhagen; Ulrich Lehmann; Hugo R. de Jonge; Mark Donowitz; C. Chris Yun; Edward J. Weinman; Olivier Kocher; Boris M. Hogema; Ursula Seidler
The epithelial anion channel CFTR interacts with multiple PDZ domain-containing proteins. Heterologous expression studies have demonstrated that the Na+/H+ exchanger regulatory factors, NHERF1, NHERF2, and PDZK1 (NHERF3), modulate CFTR membrane retention, conductivity, and interactions with other transporters. To study their biological roles in vivo, we investigated CFTR-dependent duodenal HCO3- secretion in mouse models of Nherf1, Nherf2, and Pdzk1 loss of function. We found that Nherf1 ablation strongly reduced basal as well as forskolin-stimulated (FSK-stimulated) HCO3- secretory rates and blocked beta2-adrenergic receptor (beta2-AR) stimulation. Conversely, Nherf2-/- mice displayed augmented FSK-stimulated HCO3- secretion. Furthermore, although lysophosphatidic acid (LPA) inhibited FSK-stimulated HCO3- secretion in WT mice, this effect was lost in Nherf2-/- mice. Pdzk1 ablation reduced basal, but not FSK-stimulated, HCO3- secretion. In addition, laser microdissection and quantitative PCR revealed that the beta2-AR and the type 2 LPA receptor were expressed together with CFTR in duodenal crypts and that colocalization of the beta2-AR and CFTR was reduced in the Nherf1-/- mice. These data suggest that the NHERF proteins differentially modulate duodenal HCO3- secretion: while NHERF1 is an obligatory linker for beta2-AR stimulation of CFTR, NHERF2 confers inhibitory signals by coupling the LPA receptor to CFTR.
Pflügers Archiv: European Journal of Physiology | 2009
N. Broere; Mingmin Chen; Ayhan Cinar; Anurag Singh; Jutta Hillesheim; Brigitte Riederer; Maria Lünnemann; I. Rottinghaus; Anja Krabbenhöft; Regina Engelhardt; Brigitte Rausch; E. J. Weinman; Mark Donowitz; Ann L. Hubbard; Olivier Kocher; H.R. de Jonge; Boris M. Hogema; Ursula Seidler
We investigated the role of the Na+/H+ exchanger regulatory factor 1 (NHERF1) on intestinal salt and water absorption, brush border membrane (BBM) morphology, and on the NHE3 mRNA expression, protein abundance, and transport activity in the murine intestine. NHERF1-deficient mice displayed reduced jejunal fluid absorption in vivo, as well as an attenuated in vitro Na+ absorption in isolated jejunal and colonic, but not of ileal, mucosa. However, cAMP-mediated inhibition of both parameters remained intact. Acid-activated NHE3 transport rate was reduced in surface colonocytes, while its inhibition by cAMP and cGMP was normal. Immunodetection of NHE3 revealed normal NHE3 localization in the BBM of NHERF1 null mice, but NHE3 abundance, as measured by Western blot, was significantly reduced in isolated BBM from the small and large intestines. Furthermore, the microvilli in the proximal colon, but not in the small intestine, were significantly shorter in NHERF1 null mice. Additional knockout of PDZK1 (NHERF3), another member of the NHERF family of adaptor proteins, which binds to both NHE3 and NHERF1, further reduced basal NHE3 activity and caused complete loss of cAMP-mediated NHE3 inhibition. An activator of the exchange protein activated by cAMP (EPAC) had no effect on jejunal fluid absorption in vivo, but slightly inhibited NHE3 activity in surface colonocytes in vitro. In conclusion, NHERF1 has segment-specific effects on intestinal salt absorption, NHE3 transport rates, and NHE3 membrane abundance without affecting mRNA levels. However, unlike PDZK1, NHERF1 is not required for NHE3 regulation by cyclic nucleotides.
Gastroenterology | 2009
Penghong Song; Zhe Feng; Brigitte Riederer; Anja Krabbenhöft; Brigitte Rausch; Matthias Anstätt; Heike Bantel; Jutta Lamlé; Arndt Vogel; Manoocher Soleimani; Gary E. Shull; Marian L. Miller; Ursula Seidler
Background: Recent investigations have revealed the expression of a multitude of basolateral acid/base transporters in gastric parietal cells, but the physiological significance of many of them is not established. Aim and methods: The study was designed to elucidate the physiological role of the Na/HCO3 cotransporter pNBC1, the Na+/H+ exchangers NHE1 and NHE2, all abundantly expressed in parietal cells. Isolated gastric mucosae from ten days old mice (as both NBC1and NHE1-deficient mice have a short life expectancy) were placed in classical Ussing chambers and basal and forskolin-stimulated acid secretory rate determined by back titration. Identical experiments were performed with selective pharmacological inhibitors of NBC and NHEs. Parietal cell ultrastructure was examined by electron microscopy, expression of H+/K+ATPase was assessed by quantitative RT-PCR and immunohistochemistry, epitheial cell apoptosis assessed by the TUNEL assay, and proliferation by immunohistochemistry with anti-Ki67, anti-histone. Results: Forskolin-stimulated acid secretion was significantly reduced (by >50%) in NBC1-deficient gastric mucosa, or after pharmacological inhibition of NBC1, but remained unaltered in NHE1or Slc26a7 deficient gastric mucosa in ten days old mice, or after pharmacological inhibition of NHE1 and NHE2. Parietal cell number, ultrastructure, H+/K+-ATPase expression and epithelial cell proliferation were normal in NBC1as well as NHE1 deficient mice. This indicates that pNBC1 likely serves as an additional base extrusion pathway in addition to the Cl/HCO3 exchanger AE2. In contrast, NHE2-deficient mucosae secreted acid only as a short burst, and displayed a reduction of H+/K+-ATPase but not AE2 expression. At postnatal day 10, no difference in apoptotic rate, proliferative indices, histology, and parietal cell numbers were detected in NHE2 +/+ and -/mice, whereas a complete change of the gastric proliferative zone and marked loss of parietal cell number was seen in adult stomach. Summary and conclusions: The electrogenic Na/HCO3 cotransporter NBC1 is an important base extruder during stimulation of acid secretion, and its absence or inhibition leads to a significant reduction in maximal acid secretory rates. In contrast, NHE1 and SLC26a7 anion transporter are not essential components of the ion transport machinery for gastric acid secretion in young mice. NHE2 ablation leaves parietal cell structure intact in young mice, but renders them non-functional.
The FASEB Journal | 2014
Xuemei Liu; Brigitte Riederer; Pinelopi Anagnostopoulou; Taolang Li; Brigitte Rausch; Julia Duerr; Manoocher Soleimani; Marcus A. Mall; Ursula Seidler
Proceedings of The Physiological Society | 2011
Fang Xiao; Junhua Li; Ayesha Sultan; Jian Wang; Brigitte Riederer; Regina Engelhardt; Brigitte Rausch; Georg Lamprecht; H De Jonge; Bob J. Scholte; Ursula Seidler
Gastroenterology | 2011
Brigitte Riederer; Anurag K. Singh; Sunil Yeruva; Ayesha Sultan; Brigitte Rausch; Regina Engelhardt; C. Chris Yun; Olivier Kocher; Mark Donowitz; Boris M. Hogema; Hugo deJonge; Ursula Seidler
Gastroenterology | 2011
Fang Xiao; Junhua Li; Ayesha Sultan; Jian Wang; Brigitte Riederer; Regina Engelhardt; Brigitte Rausch; Georg Lamprecht; Hugo R. de Jonge; Bob J. Scholte; Ursula Seidler
Gastroenterology | 2010
Anurag K. Singh; Brigitte Riederer; Anja Krabbenhoeft; Janina Bonhagen; Brigitte Rausch; Regina Engelhardt; Manoocher Soleimani; Ursula Seidler
The FASEB Journal | 2009
Mingmin Chen; Jeppe Praetorius; Jian Wang; Wen Zheng; Brigitte Riederer; Anja Krabbenhöft; Janina Bonhagen; Brigitte Rausch; Regina Engelhardt; Ulrike Dringenberg; Christian Aalkjaer; Ursula Seidler
Gastroenterology | 2009
Anurag K. Singh; Brigitte Riederer; Anja Krabbenhöft; Brigitte Rausch; Janina Bonhagen; Ulrike Dringenberg; Regina Engelhardt; Clifford W. Schweinfest; Manoocher Soleimani; Michael P. Manns; Ursula Seidler