Transgenic mice overexpressing the shortest human tau isoform develop a progressive tauopathy

2001 ◽  
pp. 61-69
Author(s):  
Takeshi Ishihara ◽  
Ming Hong ◽  
Bin Zhang ◽  
John Q. Trojanowski ◽  
Virginia M.-Y. Lee
Keyword(s):  
Transgenic Mice ◽  
Tau Isoform

P3-249 Possible functions of human 3 repeat tau isoform in transgenic mice with regionally specific expression

2004 ◽  
Vol 25 ◽  
pp. S425
Author(s):  
Naruhiko Sahara ◽  
Tatsuya Mizoroki ◽  
Yoshitaka Tatebayashi ◽  
Koko Ishizuka ◽  
De-Hua Chui ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Specific Expression ◽  
Tau Isoform

scholarly journals Age-Dependent Emergence and Progression of a Tauopathy in Transgenic Mice Overexpressing the Shortest Human Tau Isoform

Neuron ◽  
1999 ◽  
Vol 24 (3) ◽  
pp. 751-762 ◽  
Author(s):  
Takeshi Ishihara ◽  
Ming Hong ◽  
Bin Zhang ◽  
Yasushi Nakagawa ◽  
Michael K Lee ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Age Dependent ◽  
Tau Isoform

scholarly journals Filamentous Tau in Oligodendrocytes and Astrocytes of Transgenic Mice Expressing the Human Tau Isoform with the P301L Mutation

2003 ◽  
Vol 162 (1) ◽  
pp. 213-218 ◽  
Author(s):  
Wen-Lang Lin ◽  
Jada Lewis ◽  
Shu-Hui Yen ◽  
Michael Hutton ◽  
Dennis W. Dickson
Keyword(s):  
Transgenic Mice ◽  
P301l Mutation ◽  
Tau Isoform

scholarly journals Somatodendritic localization and hyperphosphorylation of tau protein in transgenic mice expressing the longest human brain tau isoform.

1995 ◽  
Vol 14 (7) ◽  
pp. 1304-1313 ◽  
Author(s):  
J. Götz ◽  
A. Probst ◽  
M.G. Spillantini ◽  
T. Schäfer ◽  
R. Jakes ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Human Brain ◽  
Tau Protein ◽  
Tau Isoform

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

Transgenic Mice

1992 ◽  
Vol 25 (5) ◽  
pp. 1017-1026 ◽  
Author(s):  
Rick A. Friedman ◽  
Allen F. Ryan
Keyword(s):  
Transgenic Mice
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