Ask about this productRelated genes to: FGF9 protein
- 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: FGF9 protein
Related articles to: FGF9 protein
- 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 - - Source: PubMed
Publication date: 2026/07/29
Qian JinGe LujieLu CongcongHan XiaoLi MaoqiangBian Zhenyu - Polystyrene nanoplastics (PS-NPs) are extensively present in the environment. Population studies have confirmed the presence of micro- and nanoplastics in human blood and placental tissues, and animal experiments found PS-NPs had potential developmental and reproductive toxicity. However, the continuous effects of prenatal PS-NPs exposure on testicular differentiation and development in offspring from embryo to adult are not clear. Therefore, this study aimed to investigate potential toxicity of prenatal exposure to PS-NPs on testicular development in offspring mice from embryonic day 11.5 (E11.5) to postnatal day 90 (PND90). Results showed that PS-NPs led to limited growth during embryonic period. After birth, PS-NPs caused catch-up growth, early onset of puberty, and reduced male reproductive capacity in adult mice. Moreover, we conducted further research on the possible mechanisms and found that PS-NPs might cause male reproductive developmental toxicity by inhibiting mRNA levels of genes related to testicular differentiation and development (Sry/Sox9/Fgf9, AMH, Dmrt1) from embryo to adulthood, which might have relationships with reduced number of Sertoli cells in the seminiferous tubules. Also, PS-NPs interfered with testosterone synthesis and disturbed lipid metabolism according to our proteomic analysis. This research may provide more evidence to the possible male developmental and reproductive toxicity induced by PS-NPs. - Source: PubMed
Publication date: 2025/11/19
Zhao MoxuanXie JunhongWang JingjingZhang YueXue JinglongZhang RuxuanZhang RuiyangGe WeiRen LihuaWang HongouZhou Xianqing - In brief: Fibroblast Growth Factor 9 (FGF9) binding to FGF receptor 1 activates transcription of Stard1, Scarb1, and Srd5a1 through increasing the H3K4me3 level in Leydig cells, then stimulates secretion of testosterone. Abstract: Fibroblast Growth Factor 9 (FGF9), as one of the Fibroblast Growth Factor family, is vital for testis formation. Additionally, histone modifications, especially H3K4me3, have been reported to be important in steroidogenesis. However, the regulation of stem Leydig cells differentiation by FGF9 and the role of histone modifications in this process remain unclear. Adult male Sprague-Dawley rats were treated with ethane dimethane sulfonate to deplete Leydig cells (LCs), followed by intratesticular injection of FGF9 from post-ethanedimethane sulfonate (EDS) day 14-28 at 0, 10, and 100 ng/testis. Quantitative real-time PCR and western blot analyses were used to detect the gene expression and protein levels of testosterone (T) synthesis. Chromatin immunoprecipitation sequencing (ChIP-seq) was employed to identify the H3K4me3-binding regions and binding levels. The results showed that FGF9 treatment led to an increase in serum T levels, LC number and the expression of LC-specific genes (Lhr, Scarb1, Stard1, Cyp11a1, Cyp17a1, Hsd17b3, and Hsd11b1). FGF9 markedly increased H3K4me3 protein levels and decreased H3K9me3 protein level. FGF9 promoted H3K4me3 on the promoter regions of Scarb1, Stard1, and Srd5a1 in vivo. In vitro studies demonstrated that FGF9 increased medium T levels and stimulated the incorporation of EdU, a marker of cell proliferation, into stem LCs after tubule culture. Moreover, Fgfr1 siRNA and WDR5-0103, the histone methyltransferases, could reverse the effect of FGF9 on promoting T production. This study supports previous ones demonstrating that FGF9 stimulates the proliferation and differentiation of stem LCs in an EDS-treated model and in vitro tubule culture model through H3K4me3 histone modifications. - Source: PubMed
Quan HehuaHe JiayiWang FeiluXu YubinZhang HuiqianWang QingyuanGe Ren-ShanLi Xiaoheng