Human FGF9 ELISA kit
- Known as:
- Human FGF9 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- lf-ek50041
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Human FGF9 ELISA kit
Related genes to: Human FGF9 ELISA kit
- Gene:
- FGF9 NIH gene
- Name:
- fibroblast growth factor 9
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 13q12.11
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-15
- Date modifiied:
- 2016-10-05
Related products to: Human FGF9 ELISA kit
Related articles to: Human FGF9 ELISA kit
- - Source: PubMed
- Age-related cataract (ARC) is the most prevalent form of cataract. Oxidative stress-induced apoptosis of lens epithelial cells (LECs) is a major pathogenic factor, but its underlying molecular mechanisms remain incompletely understood. This study investigated the roles of FGF9, ERK, and MMP9 in ARC and examined whether the FGF9/ERK/MMP9 pathway is involved in the protective effects of (-)-epigallocatechin-3-gallate (EGCG) against LEC apoptosis. FGF9 and MMP9 were downregulated at both the mRNA and protein levels in ARC mice and HO (200 µM)-treated HLE-B3 cells as determined by immunohistochemistry, Western blotting and qRT-PCR. FGF9 overexpression increased cell viability and reduced apoptosis in HO-treated HLE-B3 cells, as demonstrated by CCK-8 and Hoechst 33342 staining. EGCG treatment improved cell viability and increased FGF9 expression in HO-treated cells and lens tissues from ARC mice. Conversely, FGF9 knockdown attenuated the protective effect of EGCG. Further experiments suggested that FGF9 may contribute to the anti-apoptotic effects of EGCG by modulating ERK phosphorylation and MMP9 expression. ERK activation by TBHQ increased the viability of HO-treated HLE-B3 cells, whereas ERK inhibition with PD98059 attenuated the protective effects of EGCG and decreased MMP9 expression. Moreover, MMP9 knockdown increased cleaved caspase-9 expression and was accompanied by increased apoptosis in LECs. These findings suggest that the FGF9/ERK/MMP9 pathway is involved in oxidative stress-induced LEC apoptosis and may contribute, at least in part, to the protective effects of EGCG in experimental models of ARC. - Source: PubMed
Yu JialeWu YifanWu JiananShi CuigeChen XiaofengWei YingGuan LinaHe JialingZhang YueXiang ZihanSu DongmeiHu ShanshanMa Xu - Baricitinib, a selective JAK1/JAK2 inhibitor with established anti-inflammatory properties, has demonstrated therapeutic efficacy in several autoimmune and inflammatory diseases. This study aimed to investigate the neuroprotective potential of baricitinib in a ketamine-induced rat model of schizophrenia. Specifically, the study examined its effects on behavioral deficits, neurochemical alterations, and neuroinflammatory responses, while exploring the association of the JAK2/STAT3 and PI3K/AKT/mTOR signaling pathways with its neuroprotective effects. Schizophrenia-like symptoms were induced by intraperitoneal administration of ketamine (30 mg/kg) for five consecutive days, followed by oral treatment with baricitinib (5 or 20 mg/kg/day) for 14 days. Ketamine administration produced significant locomotor hyperactivity, social withdrawal, and cognitive impairment, accompanied by reduced dopamine D2 receptor (D2R), contrary to elevating fibroblast growth factor 9 (FGF9), NLRP3 expression, and pro-inflammatory cytokines including interleukin-1β, interleukin-6, and tumor necrosis factor-α in both the hippocampus and prefrontal cortex. These changes were associated with marked hyperactivation of the JAK2/STAT3 and PI3K/AKT/mTOR pathways. Treatment with baricitinib, particularly at the higher dose (20 mg/kg), significantly attenuated behavioral deficits, restored D2R expression, suppressed FGF9 and NLRP3 levels, reduced pro-inflammatory cytokine production, and normalized aberrant signaling pathway activation. Histological analysis further confirmed preservation of neuronal integrity in both brain regions. These findings indicate that baricitinib exerts robust neuroprotective effects in a ketamine model of schizophrenia, accompanied by attenuation of neuroinflammation and modulation of the JAK/STAT and PI3K/AKT/mTOR pathways. The present results suggest that baricitinib may represent a promising therapeutic candidate for mitigating neuroimmune dysregulation associated with schizophrenia-like alterations. - Source: PubMed
Publication date: 2026/08/19
Albariqi Ali ANawwar Dalia AIbrahim Weam WKhattab Mahmoud M - Environmental toxicants (ENVOTOX) have emerged as critical risk factors for congenital malformations (CMFs) in the modern industrial era. Although epidemiological evidence underscores their adverse impact on pregnancy outcomes, the underlying molecular mechanisms remain insufficiently defined. This review consolidates current insights into exposome toxicity profiling, developmental pathway disruptions, and molecular mapping to identify potential biomarkers and mechanistic links between ENVOTOX and CMFs. Protein-protein interaction (PPI) network analysis identified 35 CMF-associated proteins, with ten fibroblast growth factors (FGFs: FGF4, FGF5, FGF8, FGF9, FGF10, FGF16, FGF17, FGF18, FGF20, and FGF22) prioritized as hub nodes. Molecular docking analysis showed high binding affinity of FGF9 and FGF4 toward dioxin-associated toxicants, with dibenzo-p-dioxin (DBPDO) exhibiting the strongest interaction (binding energy: -7.2 kcal/mol), followed by polychlorinated dibenzofurans (PCDBFs) (-6.7 kcal/mol) with FGF9. Notably, FGF9 exhibited mutagenic binding potential at ASN146, mediated through π-donor hydrogen bonding with DBPDO. Comparative toxicity data further highlighted the acute risks, as DBPDO demonstrated a lower LD (2.26 mol/kg) relative to PCDBFs (4.134 mol/kg). Collectively, this review emphasizes the central role of FGFs in mediating ENVOTOX-induced teratogenicity and offers molecular-level perspectives to guide biomarker discovery and intervention strategies for mitigating CMF risk. - Source: PubMed
Shukla Adarsh KumarMahajan RashmiTyagi Anuj KumarSwaroop Kamendra - Wound-induced hair follicle neogenesis (WIHN) represents a remarkable regenerative phenomenon observed in adult mammalian skin (predominantly studied in mice), in which large full-thickness wounds bypass fibrotic scarring to generate fully functional hair follicles. This process reflects the context-dependent reactivation of embryonic morphogenetic programs, driven by a coordinated tripartite immune-microbial-epithelial axis (defined here as the integrated multi-directional signaling network among localized immune cells, epithelial stem cells, and the skin microbiota/fibroblasts). Mechanistically, γδ T cells initiate dermal fibroblast reprogramming through an FGF9-Wnt feed-forward loop, while macrophages promote AKT/β-catenin signaling in Lgr5 epithelial stem cells via TNF-α-driven non-canonical pathways. Regulatory T cells (Tregs) further support follicular morphogenesis by delivering Jagged1/Notch signals. In parallel, the skin microbiota acts as a key amplifier of regeneration, modulating the wound microenvironment through the IL-1β/MyD88 signaling axis. Taken together, WIHN illustrates the remarkable functional plasticity of immune signaling, which can be repurposed from host defense to orchestrating tissue regeneration. By elucidating this dynamic murine skin-immune dialogue, this mini-review provides a conceptual framework for speculative precision immunomodulatory therapies and emerging translational approaches-such as laser-assisted tissue remodeling-aimed at treating inflammatory and scarring alopecia, as well as achieving scarless and functionally restorative wound healing. - Source: PubMed
Publication date: 2026/07/15
Ma Ying-MingShen WeiXie Xiao-LeiTang Shun-LiWu YuanZhong Hua-JieYan QiangSun Hui