Cholinergic regulation of neurite outgrowth from isolated chick sympathetic neurons in culture

Small, David H.; Reed, G.; Whitefield, Bryony; Nurcombe, Victor

doi:10.1523/jneurosci.15-01-00144.1995

Cited by 150 publications

(109 citation statements)

References 44 publications

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“…Our previous studies have shown that substrate-bound laminin can stimulate neurite outgrowth in the presence of exogenously added NGF, provided that cells are cultured for longer than 6 h in a serum-free medium (Small et al, 1995). The effect of MCF-7 conditioned medium on neurite outgrowth from sympathetic neurons cultured on laminin was compared with that triggered by NGF (Figure 4).…”

Section: Biologically Active Ngf Is Released By Breast Cancer Cellsmentioning

confidence: 99%

Nerve growth factor overexpression and autocrine loop in breast cancer cells

et al. 2003

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We show here that nerve growth factor (NGF), the canonical neurotrophic factor, is synthesized and released by breast cancer cells. High levels of NGF transcript and protein were detected in breast cancer cells by reverse transcription-PCR, Western blotting, ELISA assay and immunohistochemistry. Conversely, NGF production could not be detected in normal breast epithelial cells at either the transcriptional or protein level. Confocal analysis indicated the presence of NGF within classical secretion vesicles. Breast cancer cell-produced NGF was biologically active, as demonstrated by its ability to induce the neuronal differentiation of embryonic neural precursor cells. Importantly, the constitutive growth of breast cancer cells was strongly inhibited by either NGF-neutralizing antibodies or K-252a, a pharmacological inhibitor of NGF receptor TrkA, indicating the existence of an NGF autocrine loop. Together, our data demonstrate the physiological relevance of NGF in breast cancer and its potential interest as a marker and therapeutic target.

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Section: Biologically Active Ngf Is Released By Breast Cancer Cellsmentioning

confidence: 99%

Nerve growth factor overexpression and autocrine loop in breast cancer cells

et al. 2003

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“…To determine the amount of neurite outgrowth, cells were viewed using a phasecontrast microscope and neurite length was measured by computer-assisted image capture analysis as described by Small et al (1995). Nine fields, each containing approximately five to…”

Section: Culture and Analysis Of Chick Sympathetic Neuronsmentioning

confidence: 99%

Substrate‐Bound β‐Amyloid Peptides Inhibit Cell Adhesion and Neurite Outgrowth in Primary Neuronal Cultures

Postuma

Nunan

et al. 2000

Journal of Neurochemistry

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Accumulation of the ␤-amyloid protein (A␤) in the brain is an important step in the pathogenesis of Alzheimer's disease. However, the mechanism of A␤ toxicity remains unclear. A␤ can bind to the extracellular matrix, a structure that regulates adhesive events such as neurite outgrowth and synaptogenesis. The binding of A␤ to the extracellular matrix suggests that A␤ may disrupt cell-substrate interactions. Therefore, the effect of substrate-bound A␤ on the growth of isolated chick sympathetic and mouse cortical neurons was examined. A␤1-40 and A␤1-42 had dose-dependent effects on cell morphology. When tissue culture plates were coated with 0.1-10 ng/well A␤, neurite outgrowth increased. Higher amounts of A␤ peptides (Ն3 g/well) inhibited outgrowth. The inhibitory effect was related to aggregation of the peptide, as preincubation of A␤1-40 for 24 h at 37°C (a process known to increase amyloid fibril formation) was necessary for inhibition of neurite outgrowth. A␤29 -42, but not A␤1-28, also inhibited neurite outgrowth at high concentrations, demonstrating that the inhibitory domain is located within the hydrophobic C-terminal region. A␤1-40, A␤1-42, and A␤29 -42 also inhibited cell-substrate adhesion, indicating that the effect on neurite outgrowth may have been due to inhibition of cell adhesion. The results suggest that accumulation of A␤ may disrupt celladhesion mechanisms in vivo.

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“…Studies in cultured neuronal cells have shown that binding of monoclonal antibody to AChE reduces neurite outgrowth [3], suggesting a morphogenic role for AChE. Inhibition of AChE activity in neuronal cultures has no effect on neurite outgrowth if the inhibitor binds at the bottom of the active site gorge, for example when the inhibitor is diisopropylfluorophosphate [3,30]. However, an inhibitor that binds near the surface of the AChE protein, at the peripheral site, inhibits neunte outgrowth [3,15,23,28,32].…”

Section: Role Of Ache In Developmentmentioning

confidence: 99%

“…Overstimulation of these receptors may lead to respiratory failure and death. AChE has been proposed to have a second function independent of its catalytic activity [1][2][3][4]9,11,[13][14][15][16]23,25,26,28,[30][31][32], possibly serving as a cell adhesion factor in morphogenesis…”

Section: Introductionmentioning

confidence: 99%

Biochemical Markers for Exposure to Low Doses of Organophosphorus Insecticides

Lockridge¹

2002

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302, and to the Office of Management and Budget, Paperwork Reduction Project (0704-0188), Washington, DC 20503 AGENCY USE ONLY (Leave blank)2. REPORT DATE August 2 0 02 REPORT TYPE AND DATES COVEREDAnnual (1 Aug 01 -31 Jul 02) TITLE AND SUBTITLE Biochemical Markers for Exposure to Low Doses of Organophosphorus Insecticides AUTHOR(S)Oksana Lockridge, Ph.D. FUNDING NUMBERS DAMD17-01-1-0776 PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)University of Nebraska Medical Center Omaha, Nebraska 68198-6810 E-Mail: olockrid@unmc.edu Though acetylcholinesterase is the primary target of organophosphorus toxicants, our finding that acetylcholinesterase knockout mice are supersensitive to the lethal effects of VX, DFP, chlorpyrifos oxon, and iso-OMPA demonstrates that other important targets exist. The goal of this work is to identify non-acetylcholinesterase targets of organophosphorus toxicants. PERFORMING ORGANIZATION REPORT NUMBER SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES)UBiotinylated-organophosphate was used to label proteins in mouse brain.The labeled proteins were separated by polyacrylamide gel electrophoresis and visualized with avidin conjugated to a fluorophore.This method has yielded 29 organophosphorus-reactive protein bands in mouse brain.They range in size from 15 to 100 kDa.Rate constants for reaction with biotinylated organophosphate were measured for the 29 proteins as well as for purified human acetylcholinesterase and human butyrylcholinesterase.A method has been developed to screen proteins for reactivity with organophosphorus agents.This work is expected to identify new biological markers for low dose exposure to organophosphorus toxicants and to explain the neurologic symptoms of some of our Gulf War veterans. Introduction. The purpose of this work is to identify proteins that react with low doses of organophosphorus agents (OP). There is overwhelming evidence that acute toxicity of OP is due to inhibition of AChE. However, we have found that the AChE knockout mouse, which has zero AChE, is supersensitive to low doses of OP. The AChE -/-mouse dies at doses of OP that are not lethal to wild-type mice (Duysen et al., 2001;Duysen et al., 2002). This demonstrates that non-AChE targets are involved in OP toxicity. Our goal is to identify new biological markers of exposure to organophosphorus agents. Our strategy uses biotinylated OP to label proteins, which are then visualized with avidin conjugated to a fluorophore....

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Cholinergic regulation of neurite outgrowth from isolated chick sympathetic neurons in culture

Cited by 150 publications

References 44 publications

Nerve growth factor overexpression and autocrine loop in breast cancer cells

Nerve growth factor overexpression and autocrine loop in breast cancer cells

Substrate‐Bound β‐Amyloid Peptides Inhibit Cell Adhesion and Neurite Outgrowth in Primary Neuronal Cultures

Biochemical Markers for Exposure to Low Doses of Organophosphorus Insecticides

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