Enhancing Open Data Sharing for Functional Genomics Experiments: Measures to Quantify Genomic Information Leakage and File Formats for Privacy Preservation
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PROVIDER: PRJNA915778 | ENA |
REPOSITORIES: ENA
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Project description:Enhancing Open Data Sharing for Functional Genomics Experiments: Measures to Quantify Genomic Information Leakage and File Formats for Privacy Preservation
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Project description:Angiogenesis is an essential process in human physiology and disease pathology. Particularly, in ischemic disease condition, the proper induction of angiogenesis without vascular leakage will be crucial for its effective therapy. Ginsenosides, triterpenoid saponins from a well-known medicinal plant ginseng, have been considered as a strong candidate for modulating angiogenesis. However, the biologic activity of individual gensenoside compounds and their target pathway have not been elucidated systematically. To find the candidates of vascular-related therapeutic agents, we evaluated in vitro angiogenic efficacy of 10 ginsenosides using tube formation assay with human umbilical vein endothelial cells (HUVECs). Among them, F1 and Rh1 showed strong in vitro angiogenic properties including EC tube formation, proliferation, and migration similar to vascular endothelial growth factor (VEGF). However, RNA transcriptome analysis showed that F1 and Rh1 differentially regulate gene expressions in HUVECs compared to VEGF. Not only that, F1 and Rh1 significantly inhibited vascular endothelial growth factor (VEGF)-induced vascular leakage both in vitro and in vivo. From RNA transcriptome analysis, we identified that nuclear receptor subfamily 4 group A member 1 (NR4A1) is regulated by F1 and Rh1 for suppression of VEGF-induced vascular leakage. By suppressing the expression and transcriptional activity of NR4A1, F1 and Rh1 could stabilize the expression and localization of junctional vascular endothelial (VE)-cadherin. These findings demonstrate that F1 and Rh1 could be potential compounds in the development of vascular pharmaceuticals.
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Project description:Ehrenstein1997 - The choline-leakage
hypothesis in Alzheimer's disease
This model is described in the article:
The choline-leakage
hypothesis for the loss of acetylcholine in Alzheimer's
disease.
Ehrenstein G, Galdzicki Z, Lange
GD.
Biophys. J. 1997 Sep; 73(3):
1276-1280
Abstract:
We present a hypothesis for the loss of acetylcholine in
Alzheimer's disease that is based on two recent experimental
results: that beta-amyloid causes leakage of choline across
cell membranes and that decreased production of acetylcholine
increases the production of beta-amyloid. According to the
hypothesis, an increase in beta-amyloid concentration caused by
proteolysis of the amyloid precursor protein results in an
increase in the leakage of choline out of cells. This leads to
a reduction in intracellular choline concentration and hence a
reduction in acetylcholine production. The reduction in
acetylcholine production, in turn, causes an increase in the
concentration of beta-amyloid. The resultant positive feedback
between decreased acetylcholine and increased beta-amyloid
accelerates the loss of acetylcholine. We compare the
predictions of the choline-leakage hypothesis with a number of
experimental observations. We also approximate it with a pair
of ordinary differential equations. The solutions of these
equations indicate that the loss of acetylcholine is very
sensitive to the initial rate of beta-amyloid production.
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2024-09-02 | BIOMD0000000553 | BioModels