Regulation of the Human Neurofilament Light and Heavy Genes in Transgenic Mice

1992 ◽  
pp. 201-208
Author(s):  
G. Charron ◽  
L. Beaudet ◽  
E. Côté ◽  
D. Houle ◽  
J.-P. Julien
Keyword(s):  
Transgenic Mice ◽  
Neurofilament Light

Origin of the two mRNA species for the human neurofilament light gene

1992 ◽  
Vol 70 (5) ◽  
pp. 279-284 ◽  
Author(s):  
Lucille Beaudet ◽  
Guy Charron ◽  
Jean-Pierre Julien
Keyword(s):  
Transgenic Mice ◽  
Rna Processing ◽  
Transcription Initiation ◽  
Northern Blotting ◽  
Proximal Promoter ◽  
Neurofilament Light ◽  
Mrna Species ◽  
Major Species ◽  
Flanking Regions ◽  
Polyadenylation Signals

The human neurofilament light (hNF-L) gene yields two major species of mRNAs of 2.4 and 3.8 kilobases (kb) in size. To investigate the origin of these two mRNAs, we have analyzed in transgenic mice the expression of hNF-L DNA fragments including different lengths of 5′ -flanking regions. The finding that the 3.8-kb mRNA species is produced by a hNF-L transgene that includes only the proximal promoter region (−0.3 kb) demonstrates that both the 2.4- and 3.8-kb mRNAs are derived from the same site of transcription initiation. Sequencing of the 3′ untranslated region of the hNF-L gene revealed the presence of multiple AATAAA polyadenylation signals. We conclude from Northern blotting experiments using probes spanning various regions of the hNF-L gene that the 2.4- and 3.8-kb mRNAs originate from the selective use of polyadenylation signals located 1.4 kb apart.Key words: neurofilament gene, polyadenylation, transgenic mice, intermediate filament gene, RNA processing.

scholarly journals Disrupted structural connectivity in ArcAβ mouse model of Aβ amyloidosis

2020 ◽  
Author(s):  
Md. Mamun Al-Amin ◽  
Joanes Grandjean ◽  
Jan Klohs ◽  
Jungsu Kim
Keyword(s):  
White Matter ◽  
Transgenic Mice ◽  
Structural Connectivity ◽  
Brain Regions ◽  
Mice Model ◽  
Network Efficiency ◽  
Fiber Density ◽  
Neurofilament Light ◽  
Diffusion Weighted Images ◽  
Network Properties

AbstractAlthough amyloid beta (Aβ) deposition is one of the major causes of white matter (WM) alterations in Alzheimer’s disease (AD), little is known about the underlying basis of WM damage and its association with global structural connectivity and network topology. We aimed to dissect the contributions of WM microstructure to structural connectivity and network properties in the ArcAβ mice model of Aβ amyloidosis.We acquired diffusion-weighted images (DWI) of wild type (WT) and ArcAβ transgenic (TG) mice using a 9.4 T MRI scanner. Fixel-based analysis (FBA) was performed to measure fiber tract-specific properties. We also performed three complementary experiments; to identify the global differences in structural connectivity, to compute network properties and to measure cellular basis of white matter alterations.Transgenic mice displayed disrupted structural connectivity centered to the entorhinal cortex (EC) and a lower fiber density and fiber bundle cross-section. In addition, there was a reduced network efficiency and degree centrality in weighted structural connectivity in the transgenic mice. To further examine the underlying neuronal basis of connectivity and network deficits, we performed histology experiments. We found no alteration in myelination and an increased level of neurofilament light (NFL) in the brain regions with disrupted connectivity in the TG mice. Furthermore, TG mice had a reduced number of perineuronal nets (PNN) in the EC.The observed FDC reductions may indicate a decrease in axonal diameter or axon count which would explain the basis of connectivity deficits and reduced network efficiency in TG mice. The increase in NFL suggests a breakdown of axonal integrity, which would reduce WM fiber health. Considering the pivotal role of the EC in AD, Aβ deposition may primarily increase NFL release, damaging PNN in the entorhinal pathway, resulting in disrupted structural connectivity.

Different posttranscriptional controls for the human neurofilament light and heavy genes in transgenic mice

1993 ◽  
Vol 18 (1-2) ◽  
pp. 23-31 ◽  
Author(s):  
Lucille Beaudet ◽  
Francine Côté ◽  
Daniel Houle ◽  
Jean-Pierre Julien
Keyword(s):  
Transgenic Mice ◽  
Neurofilament Light

P1-116: NEUROFILAMENT LIGHT LEVELS IN THE CEREBROSPINAL FLUID ARE UNCOUPLED OF AMYLOIDOSIS IN LATE STAGE PATHOGENESIS OF APP TRANSGENIC MICE

2006 ◽  
Vol 14 (7S_Part_5) ◽  
pp. P315-P315
Author(s):  
Ruth E. Droege ◽  
Stephan A. Kaeser ◽  
Juliane Schelle ◽  
Lisa M. Haesler ◽  
Rawaa Al-Shaana ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Transgenic Mice ◽  
Late Stage ◽  
Neurofilament Light ◽  
Light Levels

scholarly journals Long-Term Effects of Repetitive Mild Traumatic Injury on the Visual System in Wild-Type and TDP-43 Transgenic Mice

2021 ◽  
Vol 22 (12) ◽  
pp. 6584
Author(s):  
Kristina Pilipović ◽  
Jelena Rajič Bumber ◽  
Petra Dolenec ◽  
Nika Gržeta ◽  
Tamara Janković ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Visual System ◽  
Behavioral Problems ◽  
Optic Tract ◽  
Synaptic Organization ◽  
Wild Type ◽  
Long Term Effects ◽  
Experimental Conditions ◽  
Neurofilament Light Chain ◽  
Neurofilament Light

Little is known about the impairments and pathological changes in the visual system in mild brain trauma, especially repetitive mild traumatic brain injury (mTBI). The goal of this study was to examine and compare the effects of repeated head impacts on the neurodegeneration, axonal integrity, and glial activity in the optic tract (OT), as well as on neuronal preservation, glial responses, and synaptic organization in the lateral geniculate nucleus (LGN) and superior colliculus (SC), in wild-type mice and transgenic animals with overexpression of human TDP-43 mutant protein (TDP-43G348C) at 6 months after repeated closed head traumas. Animals were also assessed in the Barnes maze (BM) task. Neurodegeneration, axonal injury, and gliosis were detected in the OT of the injured animals of both genotypes. In the traumatized mice, myelination of surviving axons was mostly preserved, and the expression of neurofilament light chain was unaffected. Repetitive mTBI did not induce changes in the LGN and the SC, nor did it affect the performance of the BM task in the traumatized wild-type and TDP-43 transgenic mice. Differences in neuropathological and behavioral assessments between the injured wild-type and TDP-43G348C mice were not revealed. Results of the current study suggest that repetitive mTBI was associated with chronic damage and inflammation in the OT in wild-type and TDP-43G348C mice, which were not accompanied with behavioral problems and were not affected by the TDP-43 genotype, while the LGN and the SC remained preserved in the used experimental conditions.

scholarly journals Neuron Specificity of the Neurofilament Light Promoter in Transgenic Mice Requires the Presence of DNA Unwinding Elements

1995 ◽  
Vol 270 (43) ◽  
pp. 25739-25745 ◽  
Author(s):  
Guy Charron ◽  
Jean-Pierre Julien ◽  
Viviane Bibor-Hardy
Keyword(s):  
Transgenic Mice ◽  
Dna Unwinding ◽  
Neurofilament Light

Quantitative Microscopic Comparison of the Organization of the Lung in Transgenic Mice Expressing Transforming Growth Factor-α (TGF-α)

1996 ◽  
Vol 54 ◽  
pp. 14-15
Author(s):  
C. G. Plopper ◽  
C. Helton ◽  
A. J. Weir ◽  
J. A. Whitsett ◽  
T. R. Korfhagen
Keyword(s):  
Growth Factor ◽  
Pulmonary Fibrosis ◽  
Transgenic Mice ◽  
Blood Vessels ◽  
Lung Parenchyma ◽  
Lung Maturation ◽  
Alveolar Air ◽  
Parenchymal Tissue ◽  
Air Space ◽  
Conducting Airways

A wide variety of growth factors are thought to be involved in the regulation of pre- and postnatal lung maturation, including factors which bind to the epidermal growth factor receptor. Marked pulmonary fibrosis and enlarged alveolar air spaces have been observed in lungs of transgenic mice expressing human TGF-α under control of the 3.7 KB human SP-C promoter. To test whether TGF-α alters lung morphogenesis and cellular differentiation, we examined morphometrically the lungs of adult (6-10 months) mice derived from line 28, which expresses the highest level of human TGF-α transcripts among transgenic lines. Total volume of lungs (LV) fixed by airway infusion at standard pressure was similar in transgenics and aged-matched non-transgenic mice (Fig. 1). Intrapulmonary bronchi and bronchioles made up a smaller percentage of LV in transgenics than in non-transgenics (Fig. 2). Pulmonary arteries and pulmonary veins were a smaller percentage of LV in transgenic mice than in non-transgenics (Fig. 3). Lung parenchyma (lung tissue free of large vessels and conducting airways) occupied a larger percentage of LV in transgenics than in non-transgenics (Fig. 4). The number of generations of branching in conducting airways was significantly reduced in transgenics as compared to non-transgenic mice. Alveolar air space size, as measured by mean linear intercept, was almost twice as large in transgenic mice as in non-transgenics, especially when different zones within the lung were compared (Fig. 5). Alveolar air space occupied a larger percentage of the lung parenchyma in transgenic mice than in non-transgenic mice (Fig. 6). Collagen abundance was estimated in histological sections as picro-Sirius red positive material by previously-published methods. In intrapulmonary conducting airways, collagen was 4.8% of the wall in transgenics and 4.5% of the wall in non-transgenic mice. Since airways represented a smaller percentage of the lung in transgenics, the volume of interstitial collagen associated with airway wall was significantly less. In intrapulmonary blood vessels, collagen was 8.9% of the wall in transgenics and 0.7% of the wall in non-transgenics. Since blood vessels were a smaller percentage of the lungs in transgenics, the volume of collagen associated with the walls of blood vessels was five times greater. In the lung parenchyma, collagen was 51.5% of the tissue volume in transgenics and 21.2% in non-transgenics. Since parenchyma was a larger percentage of lung volume in transgenics, but the parenchymal tissue was a smaller percent of the volume, the volume of collagen associated with parenchymal tissue was only slightly greater. We conclude that overexpression of TGF-α during lung maturation alters many aspects of lung development, including branching morphogenesis of the airways and vessels and alveolarization in the parenchyma. Further, the increases in visible collagen previously associated with pulmonary fibrosis due to the overexpression of TGF-α are a result of actual increases in amounts of collagen and in a redistribution of collagen within compartments which results from morphogenetic changes. These morphogenetic changes vary by lung compartment. Supported by HL20748, ES06700 and the Cystic Fibrosis Foundation.

Eleveted serum gastrin level cannot maintain basal and stimulated gastric acid secretion in histamine deficient transgenic mice

2001 ◽  
Vol 120 (5) ◽  
pp. A180-A180
Author(s):  
B HUNYADY ◽  
A ZOLYOMI ◽  
J CZIMMER ◽  
G MOZSIK ◽  
E BUZAS ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Serum Gastrin ◽  
Gastrin Level ◽  
Serum Gastrin Level
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