FGF 2 Mouse
Description
Neurogenesis and CNS Development
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FGF-2 knockout (FGF-2⁻/⁻) mice exhibit reduced neuronal density in the motor cortex and delayed wound healing .
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HMW FGF-2 regulates cortical architecture by modulating transcription factors like NANOG and GATA4 during embryonic development .
Cardiovascular System
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FGF-2LMW knockout mice: Impaired left ventricular function, increased myocardial stiffness, and altered diastolic filling .
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FGF-2HMW overexpression: Enhances capillary density and activates mitogen-activated protein kinase (MAPK) pathways .
Bone Regeneration
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FGF-2LMW promotes osteoblast proliferation but inhibits differentiation at low concentrations (10 ng/mL) .
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HMW isoforms drive bone repair via FGFR1 signaling, with transgenic mice showing accelerated fracture healing .
Stem Cell Culture
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FGF-2 is essential for maintaining undifferentiated embryonic stem cells by suppressing differentiation via gremlin-mediated BMP inhibition .
Mental Health
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Both LMW and HMW FGF-2 isoforms reverse depression-like behaviors in chronic unpredictable mild stress (CUMS) mice by reducing oxidative stress and normalizing BDNF/FGFR1 signaling .
Disease Models
Product Specs
HBGF-2, Prostatropin, FGF-2, FGB-b.
Q&A
What are the key experimental models for studying FGF-2’s role in neurodevelopment and neurodegeneration?
Answer:
Mouse models targeting FGF-2 signaling pathways provide critical insights into its dual role in neurodevelopment and neuroprotection. Three primary models are used:
These models highlight FGF-2’s context-dependent effects: while FGF-2 −/− mice show increased DA neuron density during development, they exhibit reduced survival post-6-OHDA lesion, suggesting failed compensatory mechanisms in adulthood . Transgenic mice (TgFGF-2 +/−) demonstrate enhanced neuroprotection, indicating FGF-2’s therapeutic potential in Parkinson’s disease models .
How does FGF-2 signaling differ in neurodevelopment vs. neurodegeneration scenarios?
Answer:
FGF-2 exhibits dual roles depending on the biological context:
This dichotomy underscores the need for context-specific experimental designs:
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Developmental studies require analysis of embryonic/adult FGF-2-deficient mice.
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Neurodegeneration models should include neurotoxin (e.g., 6-OHDA, Aβ) exposure and assessments of neuroprotection/neurogenesis.
What methodological challenges arise when interpreting FGF-2 knockout vs. overexpression models?
Answer:
Interpreting FGF-2 mutant phenotypes requires addressing compensatory mechanisms and isoform-specific effects:
How does FGF-2 gene transfer enhance neurogenesis in Alzheimer’s disease models?
Answer:
FGF-2 gene delivery via AAV2/1 vectors promotes neurogenesis and Aβ clearance through multiple pathways:
AAV2/1-FGF2 injection timing is critical:
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Pre-symptomatic treatment: Prevents neurogenesis inhibition.
What contradictions exist in FGF-2’s role in neurodevelopment vs. neurodegeneration?
Answer:
FGF-2’s effects are paradoxical across developmental vs. pathological contexts:
These contradictions highlight the non-linear dose-response relationship of FGF-2, necessitating time-dependent experimental designs to disentangle developmental vs. regenerative roles.
How does FGF-2 influence cardiovascular regulation in neural circuits?
Answer:
FGF-2 is critical for central blood pressure regulation via autonomic nervous system development:
Key insight: FGF-2’s role in neural circuit formation during embryogenesis is essential for autonomic control of blood pressure, but not required for adult maintenance .
What technical considerations are critical when using FGF-2 in vitro/in vivo models?
Answer:
FGF-2’s isoform-specific activity and purity directly impact experimental outcomes:
In vivo delivery: AAV2/1-FGF2 shows efficient hippocampal targeting but requires optimization of serotype and titer to avoid off-target effects .
How does FGF-2 deficiency impact peripheral vs. central nervous system pathologies?
Answer:
FGF-2’s role varies significantly between PNS and CNS:
Key takeaway: FGF-2 is dispensable for PNS development but essential for CNS plasticity, guiding targeted therapeutic strategies in peripheral vs. central neuropathies .
What unresolved questions remain in FGF-2’s neurobiological research?
Answer:
These questions underscore the need for multi-omics approaches (e.g., single-cell RNA-seq, proteomics) to resolve FGF-2’s context-dependent signaling networks.
How should researchers validate FGF-2’s therapeutic efficacy in preclinical models?
Answer:
Therapeutic validation requires rigorous multi-parameter analysis:
Critical controls: Use dose-response curves and vehicle-injected littermates to rule out confounding variables .
Product Science Overview
FGF-2 is a single, non-glycosylated polypeptide chain. The mouse recombinant version of FGF-2 is produced in E. coli and consists of 146 amino acids, with a molecular mass of approximately 16.3 kDa . The protein is highly purified using proprietary chromatographic techniques to ensure its bioactivity and stability.
FGF-2 interacts with high-affinity transmembrane receptors, known as fibroblast growth factor receptors (FGFRs), to influence cell proliferation and tissue neovascularization . It is mitogenic for many cell types, both epithelial and mesenchymal, and shows potent angiogenic activity, which is crucial for wound healing and tissue regeneration .
Recombinant FGF-2 is widely used in cell culture applications due to its ability to promote cell growth and differentiation. It is particularly useful in the proliferation of adipose-derived mesenchymal cells and enhancing chondrogenesis in three-dimensional micromass culture . Additionally, FGF-2 has been implicated in tumor angiogenesis, making it a valuable tool in cancer research .
