Ask about this productRelated genes to: FGF20 protein
- Gene:
- FGF20 NIH gene
- Name:
- fibroblast growth factor 20
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8p22
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-19
- Date modifiied:
- 2015-09-07
Related products to: FGF20 protein
Related articles to: FGF20 protein
- Microglia play dual roles in neuroinflammation, driving either detrimental M1 or protective M2 polarization, which critically impacts the outcomes of ischemic stroke. While fibroblast growth factor 20 (FGF20) is established as a neurotrophic factor with neuroprotective properties, its role in regulating microglial polarization remains unclear. This study investigated a novel function of FGF20 in alleviating post-stroke neuroinflammation and its underlying mechanisms. In a rat model of middle cerebral artery occlusion (MCAO), intracerebroventricular administration of FGF20 significantly reduced infarct volume and improved neurological function. RT-PCR analysis revealed that FGF20 bidirectionally regulated cytokine expression, suppressing M1-associated markers (CD86, IL-1β, IL-6, iNOS, TNF-α) while enhancing M2-associated markers (IL-10, Arg-1). Immunofluorescence staining demonstrated that FGF20 attenuated microglia activation in peri-infarct striatum and hippocampus. In vitro, FGF20 counteracted LPS-induced M1 polarization in primary microglia, downregulated the TLR4/NF-κB pathway, and upregulated TREM2 expression. Notably, while the selective FGFR1 inhibitor PD173074 abolished FGF20-induced TREM2 upregulation, it did not reverse the suppression of TLR4/NF-κB, indicating that these two effects are mediated through distinct regulatory mechanisms. These phenotypic shifts were further confirmed by a reduction in CD32/16 (M1) cells and an increase in Arg1 (M2) cells. Mechanistically, FGF20 restored the balance between TREM2 and TLR4 signaling, inhibiting NF-κB activation and attenuating neuroinflammatory responses. Collectively, our findings identify FGF20 as a novel dual modulator of microglial polarization that integrates TREM2-mediated immunoregulation with FGFR1-dependent and independent suppression of TLR4/NF-κB pathway. Thus, FGF20 represents a promising therapeutic candidate for ischemic stroke, extending its functional profile from neuroprotection to targeted immunomodulation through phenotype-specific regulation of microglial polarization. - Source: PubMed
Publication date: 2026/03/08
Zhu LiyunGuo ShufeiWang ZhengyiHuang MinLiu MengfanRuan LixinZou YuchiLin LiWang Xue - The mechanisms that regulate the even spacing of placodes during embryonic development remain intriguing. These mechanisms typically involve complex interactions between signaling pathways, which can be further influenced by mechanical forces as the embryo grows. Here, we investigate the patterning of the ring of conjunctival placodes in the anterior eye of chicken embryos by functionally manipulating the BMP signaling pathway. Specifically, we electroporated a TWSG1 plasmid at HH27 to modulate BMP signaling during the pre-patterning phase and examined the effects on placode formation and key developmental pathways. Our results show that modulation of BMP signaling at HH27 influences placode development, morphology and spacing three days later, at HH34. qPCR data confirm an initial and statistically significant upregulation of FGF20 and WNT2B 6 h after electroporation. However, one day later (at HH29), only β-catenin is significantly elevated. Multiplex fluorescent in situ hybridization shows WNT2 expression in the conjunctival placodes and papillae for the first time. This WNT2 expression is colocalized with β-catenin in controls and remains spatially colocalized after electroporation. Together, these results provide functional evidence that BMP signaling regulates both canonical WNT/β-catenin and FGF pathways during early placode formation and support a model in which BMP may act as the inhibitor in a Turing-like reaction-diffusion mechanism underlying conjunctival placode patterning in the anterior eye. - Source: PubMed
Publication date: 2026/01/17
Herold AveevaFranz-Odendaal Tamara Anne - The Wnt/FGF20 axis establishes an organizing center that is largely non-proliferative in the distal blastema during epimorphic regeneration across multiple model systems. However, the underlying mechanisms remain poorly characterized. In this study, we investigate the role of the Wnt/FGF20 axis during tail regeneration in Gekko japonicus. We also developed an in vitro system to evaluate the effects of Wnt agonists, FGF20, and FGFR4 on cultured blastema cells. Our results demonstrate that Wnt signaling is activated in distal blastema cells and contributes to a lower proportion of proliferative cells beneath the epidermal basal layer in the regenerating tail of Gekko japonicus. This Wnt-mediated suppression of proliferation is associated with reduced FGFR4 expression, as confirmed both in vitro and in vivo. Furthermore, Wnt pathway activation upregulates FGF20 expression in distal blastema cells, which promotes the migration of proximal blastema cells without affecting their proliferation. Our findings provide an insight into the organizing center of regenerated tissue, revealing a reciprocal regulatory interaction between the epidermis and blastema cells during successful epimorphic regeneration. - Source: PubMed
Publication date: 2025/12/15
Xu ManLi ZhenYu JingLi MingxuanZhang YufangHuang ShuaiXu YanranChen XuWu RonghuaLiu MeiLiu Yan - Previous studies have suggested a potential association between fibroblast growth factors (FGFs) and breast cancer (BC), but the evidence for the relationship between specific FGFs with BC is limited and controversial. To explore the interactions between 13 FGFs and 3 fibroblast growth factor receptors (FGFRs) with BC and its subtypes (ER+ and ER-), we conducted a Mendelian randomization (MR) analysis based on genome-wide association study summary statistics of European ancestry. Several techniques were used to ensure the stability of the causal effect, such as inverse-variance weighting, weighted median, MR-Egger regression, and Mendelian Randomization Pleiotropy Residual Sum and Outlier. Heterogeneity was assessed by calculating the Cochran's Q value. The inverse-variance weighting analysis showed that for overall BC, FGF20 showed a genetically protective effect (odds ratio [OR] 0.996, 95% CI: 0.993-1.000, P = .027), FGF4 can genetically promote the risk of BC (OR 1.004, 95% CI: 1.001-1.007, P = .013). FGF1 (OR 1.055, 95% CI: 1.005-1.107, P = .029) and FGF7 (OR 1.068, 95% CI: 1.007-1.133, P = .028) were consistently associated with increased risk of ER+ BC, however FGF20 (OR 0.959, 95% CI: 0.920-0.999, P = .046) decreased the risk of ER+ BC. FGF23 (OR 1.077, 95% CI: 1.003-1.158, P = .042) promote the risk of ER- BC. In the reverse MR study, ER+ BC tended to exhibit elevated levels of FGF7 (OR 1.072, 95% CI: 1.004-1.144, P = .037) and decreased levels of FGFR2 (OR 0.930, 95% CI: 0.872-0.992, P = .027). Our study results indicate that only specific types of FGFs and FGFRs may have a causal relationship with BC. Th research provides a new perspective on the mechanisms of action of different types of FGFs and FGFRs in BC, and offers potential genetic support for personalized medicine and precision therapy. - Source: PubMed
Feng FubinSun MengxuanYao YanLi HuayaoSong LinqiSun Changgang - Stroke is the second leading cause of death and the primary cause of disability worldwide, yet effective treatments to restore neurological function remain limited. Fibroblast growth factor 20 (FGF20), a promising neurotrophic factor with demonstrated efficacy in neurological disorders, faces a critical translational barrier due to its poor blood-brain barrier (BBB) permeability. To address this limitation, we developed genetically engineered rabies virus glycoprotein (RVG)-modified extracellular vesicles loaded with FGF20 (RVG-FGF20-EVs) for targeted ischemic brain delivery. Systemic administration of RVG-FGF20-EVs in a mouse middle cerebral artery occlusion (MCAO) model significantly reduced infarct volume, enhanced neuroplasticity, and improved long-term functional recovery. Mechanistic investigations revealed that RVG-FGF20-EVs exhibit a distinct miRNA cargo profile, characterized by significant upregulation of miR-181b-5p. Dual-luciferase reporter assays confirmed phosphatase and tensin homolog (PTEN) as a direct target of miR-181b-5p. Our findings demonstrate that RVG-FGF20-EVs promote neuroplasticity and functional recovery post-stroke, mediated at least partially through the miR-181b-5p/PTEN pathway. This study represents the first application of engineered RVG-EVs for efficient FGF20 brain delivery for efficient FGF20 delivery, establishing their unique efficacy in treating ischemic stroke and providing a multifunctional platform for treating neurological disorders. Further optimization and standardization are needed to translate this promising platform into clinical applications. In conclusion, RVG-FGF20-EVs constitute a promising novel therapeutic strategy for ischemic stroke. - Source: PubMed
Publication date: 2025/07/30
Guo ShufeiWang ZhengyiShi RuiqingHuang PengkaiFang YaniChen ShihaoHuang MinHu JianLu YiyuanXu XinyiZou YuchiRuan LixinLi XiaokunLin LiWang Xue