EG VEGF Mouse
Description
Molecular Characterization of Mouse EG-VEGF
Mouse EG-VEGF shares 88% amino acid sequence identity with human EG-VEGF . Key features include:
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Structure: A 105-amino acid protein with 10 cysteines, structurally homologous to snake venom protein A .
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Receptor Binding: Activates G protein-coupled receptors PKR1 and PKR2, triggering calcium mobilization, phosphoinositide turnover, and MAPK signaling .
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Isoforms: Unlike VEGF-A, EG-VEGF has no splice variants but exhibits functional divergence from VEGF in angiogenesis regulation .
Table 1: Comparative Features of EG-VEGF and VEGF in Mice
Tissue-Specific Expression and Regulation
Mouse EG-VEGF exhibits unique expression dynamics:
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Primary Sites: Predominantly in hepatocytes and renal tubule cells, contrasting with human EG-VEGF's steroidogenic gland restriction .
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Promoter Differences: Lacks NR5A1-binding sites critical for steroidogenic transcription in humans, explaining divergent expression patterns .
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Hypoxia Response: Unlike VEGF, EG-VEGF expression is not directly hypoxia-inducible but correlates with inflammatory cytokines .
Endocrine Gland Angiogenesis
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Adrenal Cortex: Promotes endothelial cell proliferation and survival via PKR1/2-mediated MAPK and AKT pathways .
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Ovary/Testis: Induces angiogenesis and cyst formation without affecting non-endocrine tissues (e.g., cornea) .
Placental Development
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Microvascular Specificity: Stimulates human placental endothelial cell (HPEC) proliferation, migration, and tube formation 3x more potently than VEGF .
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Permeability Regulation: Increases transendothelial electrical resistance (TEER) by 50% and paracellular transport in HPECs .
Table 2: EG-VEGF Effects on Placental Endothelial Cells
Cancer Biology
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Tumor Angiogenesis: Upregulated in prostate and colorectal cancers, correlating with metastatic potential .
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Therapeutic Target: Anti-EG-VEGF antibodies reduce xenograft tumor growth by 40% in murine models .
Pregnancy Disorders
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Preeclampsia: Placental EG-VEGF levels drop 3-fold compared to healthy pregnancies, impairing fetomaternal angiogenesis .
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Recurrent Miscarriage: Low circulating EG-VEGF (<50 pg/mL) predicts 70% risk of early pregnancy loss .
Experimental Models and Tools
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Knockout Mice:
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Quantification Assays:
Comparative Pharmacodynamics
Product Specs
Q&A
Here’s a structured FAQ collection for researchers studying EG-VEGF in murine models, based on current scientific literature and experimental methodologies:
Advanced Research Questions
How do tissue-specific expression discrepancies between human and mouse EG-VEGF impact translational research?
Mouse EG-VEGF is predominantly expressed in liver/kidney, unlike humans (steroidogenic glands) . This divergence arises from promoter differences:
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Human EG-VEGF: Contains NR5A1 binding sites for steroidogenic regulation .
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Mouse EG-VEGF: Lacks NR5A1 sites, leading to broader expression .
Experimental Design Tip: Use humanized mouse models (e.g., hum-X VEGF KI) to reconcile species-specific pathways.
How can conflicting data on EG-VEGF’s role in tumor models be resolved?
Studies show tumor-derived VEGF contributes minimally to circulating VEGF in mice , complicating EG-VEGF’s role in oncology. Strategies:
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Parameter Estimation: Fit computational models to VEGF/VEGF Trap complex data .
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Sensitivity Analysis: Prioritize VEGF secretion rates and microvascular permeability in simulations .
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Validation: Compare EG-VEGF knockout ( Vegfb −/−) phenotypes with wild-type responses to hypoxia .
What mechanisms link PPARγ and EG-VEGF in placental development?
PPARγ directly regulates EG-VEGF transcription in mice:
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PPARγ −/− Mice: Show reduced EG-VEGF mRNA/protein in placenta, leading to vascular defects .
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In Vitro Models: Treat trophoblast cells with PPARγ agonists (e.g., rosiglitazone) to rescue EG-VEGF expression .
Data Contradiction Note: While PPARγ −/− mice die by E9.5 , Vegfb −/− mice survive but exhibit coronary vasculature defects , suggesting compensatory pathways.
Methodological Challenges
How do researchers address low EG-VEGF recovery in tissue lysates?
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Optimization Steps:
What in vivo models best recapitulate EG-VEGF’s endocrine-specific effects?
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Chorioallantoic Membrane (CAM) Assay: Mimics placental angiogenesis; anti-EG-VEGF antibodies reduce endothelial proliferation .
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Conditional Knockouts: Target Prok1 in hepatocytes/tubule cells to isolate liver/kidney phenotypes .
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Humanized Models: Introduce human EG-VEGF promoter elements into mice to study steroidogenic regulation .
Product Science Overview
EG-VEGF was first identified in 2001 as a tissue-specific angiogenic factor predominantly expressed in steroidogenic organs such as the adrenal gland, testes, ovary, and placenta . Unlike the more widely known Vascular Endothelial Growth Factor (VEGF), which is expressed in various tissues, EG-VEGF’s expression is largely restricted to endocrine glands .
The mouse ortholog of EG-VEGF shares a high degree of similarity with its human counterpart, with the cDNA and predicted amino acid sequences being 86% and 88% identical, respectively . Interestingly, the expression pattern of mouse EG-VEGF differs from that of the human protein. In mice, EG-VEGF is predominantly expressed in the liver and kidney, rather than in steroidogenic glands . This suggests that EG-VEGF may have different roles in regulating organ-specific angiogenesis in mice compared to humans.
EG-VEGF functions by binding to its receptors on the surface of endothelial cells, triggering a cascade of signaling events that lead to endothelial cell proliferation, migration, and the formation of fenestrations (small pores) in the capillary walls . This is particularly important in endocrine glands, where efficient blood supply is essential for hormone transport.
The expression of EG-VEGF is induced by hypoxia (low oxygen levels), which is a common condition in rapidly growing tissues and tumors . This hypoxia-induced expression ensures that growing tissues receive an adequate blood supply to meet their metabolic needs.
Research on EG-VEGF has provided valuable insights into the mechanisms of angiogenesis and its regulation in endocrine tissues. Studies have shown that EG-VEGF plays a critical role in the development and function of endocrine organs, as well as in pathological conditions such as tumors .
Recombinant forms of mouse EG-VEGF are used in various research applications to study its effects on endothelial cells and to explore potential therapeutic applications. For example, understanding how EG-VEGF promotes angiogenesis could lead to new treatments for diseases characterized by poor blood supply, such as ischemic heart disease and peripheral artery disease.
