FGF20 siRNA_Lentivectors
- Known as:
- FGF20 siRNA_Lentivectors
- Catalog number:
- i007903a
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FGF20 siRNA_Lentivectors
Related genes to: FGF20 siRNA_Lentivectors
- 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 siRNA_Lentivectors
Related articles to: FGF20 siRNA_Lentivectors
- Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are pathologically characterized by disruption of the alveolar-capillary barrier, excessive inflammatory responses, and dysregulated intra-pulmonary coagulation. Although inflammatory and thrombotic cascades have been extensively studied, endogenous epithelial-derived signaling mechanisms coordinating barrier stabilization with immunothrombotic restraint remain undefined. Here, we identify fibroblast growth factor 20 (FGF20) as a constitutive epithelial regulator suppressed in alveolar barrier-associated cells during sepsis-induced ALI. In a CLP rat model, both prophylactic and therapeutic administration of recombinant human FGF20 (rhFGF20) improved 7-day survival, attenuated pulmonary edema and inflammation, restored gas exchange, and preserved alveolar-capillary integrity. rhFGF20 restrained procoagulant and antifibrinolytic mediators tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) while suppressing NF-κB activation. Mechanistically, FGF20 acted through fibroblast growth factor receptor 1 (FGFR1) to engage the FGFR1-PI3K-AKT cascade. AKT activation bifurcated into two axes: (i) inhibition of NF-κB phosphorylation and nuclear translocation, restraining TF/PAI-1 transcription; and (ii) inhibitory phosphorylation of glycogen synthase kinase 3β (GSK3β) at Ser9, stabilizing epithelial and endothelial junctional proteins (E-cadherin, VE-cadherin, ZO-1). Pharmacological inhibition of FGFR1 or AKT abolished both barrier-protective and anticoagulant effects, confirming pathway dependency. Clinically, serum and bronchoalveolar lavage fluid FGF20 levels were reduced in ARDS patients and positively correlated with PaO₂/FiO₂ ratios, linking reduced FGF20 to disease severity. Collectively, these findings position FGF20 as an upstream integrator of structural and immunothrombotic homeostasis within the alveolar-capillary unit. Restoration of the FGF20-FGFR1 axis reconstitutes a proximal checkpoint stabilizing barrier architecture and constraining NF-κB-dependent procoagulant activation, highlighting FGF20 as a mechanistically grounded therapeutic target in sepsis-induced ALI/ARDS. CLINICAL SIGNIFICANCE. - Source: PubMed
Publication date: 2026/05/05
Dong QiTao JunlingYuan JiaTian JunyuanCheng YumeiWang JingniXiao ChuanChen XianjunWang YingLi WeiShen Feng - Hemodialysis (HD) patients suffer from chronic inflammation which is a serious complication and contributes significantly to morbidity and mortality. Dialysis technology has advanced over many years but despite advances, its underlying molecular mechanism remains poorly understood. We have designed an exploratory study and investigated how hemodialysis influences epigenetic changes by understanding the DNA methylation patterns which are associated with inflammation. By using the same polysulfone (PS) membrane dialyzer, we have collected the blood samples from the patients before and after dialysis. For DNA methylation analysis, we have extracted genomic DNA using the Monarch® Genomic DNA Purification Kit. Bisulfite conversion was done using the QIAGEN Epitect Bisulfite Kit. Genome Studio, which is a computational software, was used to identify the DNA methylation profiles. These profiles revealed significant epigenetic changes across the hemodialysis patients’ samples. From these DNA methylation profiles, we identified the differential methylated regions (DMRs) and focused on the genes that are associated with these DMRs with the change greater than 80% to confirm robustness. We identified the chromosomal mapping of DMR-associated genes on CpG islands and shore localization, promotor or enhancer regions, to evaluate the functional impact of methylation changes. One of the bioinformatics tools, named Discovery Annotation, Visualization, Integration Database (DAVID) was used to perform functional enrichment analysis to identify the affected biological pathways involved in neuronal signaling, immune regulation, inflammation, and metabolism. Protein- Protein Interaction network was constructed using another bioinformatics tool, named String Database, and It analysis was performed using a bioinformatics desktop-based tool called Cytoscape, which helped in identifying critical hub genes including TWIST1, SHANK3, FGF20, MEF2C, RUNX2, CAV1, CDKN2A, WNT3A, and CXCL12, which play crucial roles in immune system compromise and inflammatory regulation. A total of 93 genes, across the samples of HD patients, showed significant methylation alterations. Of which, 41 genes showed changes exceeding 100% and mostly mapped on Promoter/enhancer regions at CpG islands and shores. In HD patients, these functional consequences suggest changes in their role in impaired vascular function, cognitive decline and immune dysregulation. Fibrinogen (FB) behaviour during dialysis, particularly its adsorption onto the dialysis membranes, was understood using Synchrotron Imaging at the Canadian Light Source (CLS) which provided us a high-resolution visualization. To confirm significant FB fouling between initial and intermediate membrane layers, these targeted regions were identified using raw CT scan images and their magnified views. Similarly, we identified that the level of inflammatory biomarkers, which were elevated in post-dialysis samples of HD patients including vWF, CRP, Serpin C1, Properdin, and PF4 indicating an amplified inflammatory response. Particularly, the critical hub genes that are associated with vascular regulation including CAV1, TWIST1, CDKN2A, and CXCL1, were reported as hypermethylated after dialysis, meaning their expression may reduce which affects their contribution in endothelial dysfunction. These findings suggest a self-perpetuating inflammatory loop, where FB adsorption initiates molecular and immunological responses that reinforce epigenetic dysregulation. One of the important limiting factors is sample size, which influenced the reliability of findings across the molecular and clinical levels, and this underlines that further investigation is needed. This study helped us designed the foundational insights to target the anti-inflammatory strategies that may lead us to the development of more hemocompatible dialysis membranes to reduce long-term complications in HD patients. - Source: PubMed
Publication date: 2026/04/27
Syeda HiraBahig JumanahShoker AhmedSakharkar Meena KishoreAbdelrasoul Amira - 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