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muscarinic wnt

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https://www.readbyqxmd.com/read/27908290/bile-acid-a-potential-inducer-of-colon-cancer-stem-cells
#1
Lulu Farhana, Pratima Nangia-Makker, Evan Arbit, Kathren Shango, Sarah Sarkar, Hamidah Mahmud, Timothy Hadden, Yingjie Yu, Adhip P N Majumdar
BACKGROUND: Although the unconjugated secondary bile acids, specifically deoxycholic acid (DCA) and lithocholic acid (LCA), are considered to be risk factors for colorectal cancer, the precise mechanism(s) by which they regulate carcinogenesis is poorly understood. We hypothesize that the cytotoxic bile acids may promote stemness in colonic epithelial cells leading to generation of cancer stem cells (CSCs) that play a role in the development and progression of colon cancer. METHODS: Normal human colonic epithelial cells (HCoEpiC) were used to study bile acid DCA/LCA-mediated induction of CSCs...
December 1, 2016: Stem Cell Research & Therapy
https://www.readbyqxmd.com/read/25143365/denervation-suppresses-gastric-tumorigenesis
#2
Chun-Mei Zhao, Yoku Hayakawa, Yosuke Kodama, Sureshkumar Muthupalani, Christoph B Westphalen, Gøran T Andersen, Arnar Flatberg, Helene Johannessen, Richard A Friedman, Bernhard W Renz, Arne K Sandvik, Vidar Beisvag, Hiroyuki Tomita, Akira Hara, Michael Quante, Zhishan Li, Michael D Gershon, Kazuhiro Kaneko, James G Fox, Timothy C Wang, Duan Chen
The nervous system plays an important role in the regulation of epithelial homeostasis and has also been postulated to play a role in tumorigenesis. We provide evidence that proper innervation is critical at all stages of gastric tumorigenesis. In three separate mouse models of gastric cancer, surgical or pharmacological denervation of the stomach (bilateral or unilateral truncal vagotomy, or local injection of botulinum toxin type A) markedly reduced tumor incidence and progression, but only in the denervated portion of the stomach...
August 20, 2014: Science Translational Medicine
https://www.readbyqxmd.com/read/21914176/airway-response-to-acute-mechanical-stress-in-a-human-bronchial-model-of-stretch
#3
Christophe Faisy, Francisco M Pinto, Morgan Le Guen, Emmanuel Naline, Stanislas Grassin Delyle, Edouard Sage, Maria-Luz Candenas, Philippe Devillier
INTRODUCTION: Lung inflation may have deleterious effects on the alveoli during mechanical ventilation. However, the consequences of stretch during excessive lung inflation on basal tone and responsiveness of human bronchi are unknown. This study was undertaken to devise an experimental model of acute mechanical stretch in isolated human bronchi and to investigate its effect on airway tone and responsiveness. METHODS: Bronchi were removed from 48 thoracic surgery patients...
2011: Critical Care: the Official Journal of the Critical Care Forum
https://www.readbyqxmd.com/read/21747132/-editorial-introduction-from-the-structure-and-functions-of-the-neuromuscular-junction-to-the-diseases
#4
EDITORIAL
Masaharu Takamori
The neuromuscular junction has been recognized as a site for autoimmune and genetic disorders. Myasthenia gravis (MG) is mainly caused by postsynaptic nicotinic acetylcholine receptor (AChR) IgG1 antibodies that are directed against α-subunit 67-76 and 125-147 and activate complement. Thymic abnormalities are present in the autoimmune background. A proportion of MG patients without conformation-dependent AChR antibodies assayed by the cell-based method have muscle-specific tyrosine kinase (MuSK) antibodies which are largely IgG4 and partially IgG1...
July 2011: Brain and Nerve, Shinkei Kenkyū No Shinpo
https://www.readbyqxmd.com/read/20399743/regulation-of-gsk-3beta-and-beta-catenin-by-galphaq-in-hek293t-cells
#5
Sara Salmanian, S Mahmoud A Najafi, Maryam Rafipour, Maryam Rezaei Arjomand, Hamideh Shahheydari, Sara Ansari, Leily Kashkooli, S Javad Rasouli, Marie Saghaeian Jazi, Tayebeh Minaei
Recent studies have shown that heterotrimeric G proteins are involved in the regulation of the canonical Wnt/beta-Catenin pathway. However, the mechanism(s) behind this involvement is (are) poorly understood. Our previous results have shown that activation of Galphaq in Xenopus oocytes leads to inhibition of GSK-3beta and stabilization of the beta-Catenin protein, suggesting that Galphaq might stabilize beta-Catenin via inhibition of GSK-3beta. In this study, we have observed similar results in HEK293T cells...
May 14, 2010: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/19609278/survival-neuron-like-differentiation-and-functionality-of-mesenchymal-stem-cells-in-neurotoxic-environment-the-critical-role-of-erythropoietin
#6
L Danielyan, R Schäfer, A Schulz, T Ladewig, A Lourhmati, M Buadze, A L Schmitt, S Verleysdonk, D Kabisch, K Koeppen, G Siegel, B Proksch, T Kluba, A Eckert, C Köhle, T Schöneberg, H Northoff, M Schwab, C H Gleiter
Mesenchymal stem cells (MSCs) can ameliorate symptoms in several neurodegenerative diseases. However, the toxic environment of a degenerating central nervous system (CNS) characterized by hypoxia, glutamate (Glu) excess and amyloid beta (Abeta) pathology may hamper the survival and regenerative/replacing capacities of engrafted stem cells. Indeed, human MSC (hMSC) exposed to hypoxia were disabled in (i) the capacity of their muscarinic receptors (mAChRs) to respond to acetylcholine (ACh) with a transient increase in intracellular [Ca(2+)], (ii) their capacity to metabolize Glu, reflected by a strong decrease in glutamine synthetase activity, and (iii) their survival on exposure to Glu...
December 2009: Cell Death and Differentiation
https://www.readbyqxmd.com/read/18652670/the-role-of-wnt-signaling-in-neuronal-dysfunction-in-alzheimer-s-disease
#7
Nibaldo C Inestrosa, Enrique M Toledo
Recent evidence supports a neuroprotective role for Wnt signaling in neurodegenerative disorders such as Alzheimer's Disease (AD). In fact, a relationship between amyloid-beta-peptide (Abeta)-induced neurotoxicity and a decrease in the cytoplasmic levels of beta-catenin has been observed. Apparently Abeta binds to the extracellular cysteine-rich domain of the Frizzled receptor (Fz) inhibiting Wnt/beta-catenin signaling. Cross-talk with other signaling cascades that regulate Wnt/beta-catenin signaling, including the activation of M1 muscarinic receptor and PKC, the use of Ibuprofen-ChE bi-functional compounds, PPAR alpha, gamma agonists, nicotine and some antioxidants, results in neuroprotection against Abeta...
2008: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/15572177/signal-transduction-during-amyloid-beta-peptide-neurotoxicity-role-in-alzheimer-disease
#8
REVIEW
Rodrigo A Fuentealba, Ginny Farias, Jessica Scheu, Miguel Bronfman, María Paz Marzolo, Nibaldo C Inestrosa
Alzheimer's disease (AD) is a neurodegenerative disorder with progressive dementia accompanied by two main structural changes in the brain: intracellular protein deposits termed neurofibrillary tangles (NFT) and extracellular amyloid protein deposits surrounded by dystrophic neurites that constitutes the senile plaques. Currently, it is widely accepted that amyloid beta-peptide (A beta) metabolism disbalance is crucial for AD progression. A beta deposition may be enhanced by molecular chaperones, including metals like copper and proteins like acetylcholinesterase (AChE)...
December 2004: Brain Research. Brain Research Reviews
https://www.readbyqxmd.com/read/15474371/m1-muscarinic-receptor-activation-protects-neurons-from-beta-amyloid-toxicity-a-role-for-wnt-signaling-pathway
#9
Ginny G Farías, Juan A Godoy, Félix Hernández, Jesús Avila, Abraham Fisher, Nibaldo C Inestrosa
Amyloid-beta-peptide (Abeta) deposits are one of the hallmark features of Alzheimer's disease. Signal transduction alterations are implicate in the neuronal responses to Abeta, which include neurotransmitter systems and pathways involved in the maintenance of the nervous system. In this context, we have recently found that Abeta-neurotoxicity triggers a loss of Wnt signaling. We report here that M1-acetylcholine-muscarinic-receptor (mAChR) activation protects neurons from Abeta-toxicity. Concomitant with this effect, a modulation of the Wnt signaling was observed...
November 2004: Neurobiology of Disease
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