FGF-18, Mouse Protein
- Known as:
- FGF-18, Mouse Protein
- Catalog number:
- z03099-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- FGF-18 Mouse Protein
Related genes to: FGF-18, Mouse Protein
- Gene:
- FGF18 NIH gene
- Name:
- fibroblast growth factor 18
- Previous symbol:
- -
- Synonyms:
- FGF-18, ZFGF5
- Chromosome:
- 5q35.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-22
- Date modifiied:
- 2016-10-05
Related products to: FGF-18, Mouse Protein
Related articles to: FGF-18, Mouse Protein
- Osteoarthritis (OA) is a widespread degenerative joint condition marked by progressive cartilage breakdown, and a chronic inflammatory microenvironment, where conventional therapies largely fail to halt disease progression. To address this unmet need, an intra-articularly implantable, disease-responsive scaffold was developed for combinatorial treatment to simultaneously combat inflammation and promote anabolism. The system is based on an MMP13-sensing peptide-modified type II collagen scaffold engineered for controlled release of celecoxib (CXB), an anti-inflammatory agent, and fibroblast growth factor-18 (FGF-18), a pro-anabolic growth factor. Comprehensive physicochemical characterization confirmed the scaffold's porous structure, successful conjugation of the responsive peptide, and MMP13-dependent drug release. In vitro studies demonstrated excellent biocompatibility, potent anti-inflammatory effects, and enhanced chondrogenic matrix production under IL-1β stimulation. When evaluated the rat OA cartilage defect model, the dual-drug scaffold significantly suppressed inflammation and subchondral bone damage, while promoting early matrix anabolism, and outperforming the control group. This MMP13-sensing scaffold represents a precision medicine strategy for OA therapy, enabling intelligent, microenvironment-driven drug delivery to disrupt the degenerative cycle and facilitate synergistic early-stage anti-inflammatory and anabolic effects. - Source: PubMed
Publication date: 2026/07/13
Zhang ZhenLiu BanghengMu YuleiZhou HuiqunMa LiangXu ChenjieWang Dong-An - Diabetic foot ulcer (DFU) is a serious problem that may cause amputation of the lower extremities in patients with diabetes. The present research aimed to assess the localised tissue expression and potential immunoinflammatory crosstalk among fibroblast growth factor-18 (FGF-18), glutamic acid decarboxylase (GAD) and interleukin-35 (IL-35) in DFU compared to non-diabetic controls (NDCs), while also examining the systemic serum levels of FGF-18 and IL-35. Venous blood was collected from 80 patients with DFU and 100 NDC, and the concentrations of serum IL-35, FGF-18 and blood haemoglobin A1c (HbA1c) were analysed. Aseptically collected biopsy samples were obtained from FUs of 30 type 2 diabetes (T2D) patients and from accidental foot wounds of 30 NDC. Biopsies were preserved in formalin (10%) until paraffin blocks were prepared. The immunohistochemical methodology used antibodies specifically to identify tissue FGF-18, GAD and IL-35 in the soft tissue specimens. The tissue expression of FGF-18, IL-35 and GAD was significantly higher in DFU compared to NDC (p ≤ 0.0001), suggesting a strong localised immunoinflammatory role, whereas serum levels of FGF-18 and IL-35 remained statistically unchanged. Furthermore, significant positive correlations observed between tissue IL-35 and FGF-18 (r = 0.67, p ≤ 0.05) and between tissue IL-35 and GAD (r = 0.60, p ≤ 0.05) indicate robust immunoinflammatory crosstalk. The marked and correlated elevation of FGF-18, IL-35 and GAD specifically within DFU tissue, without changes in serum levels of FGF-18 and IL-35, establishes a robust, compartmentalised immunoinflammatory axis that drives chronic pathology and presents novel targets for localised therapeutic intervention. - Source: PubMed
Hussein Hemin MohamadAlkhuzai AhmedSmail Shukur WasmanMahwi Taha OthmanBystrom JonasJanson ChristerAmin Kawa - Non‑hematopoietic stromal cells are essential regulators of hematopoiesis; however, their contribution to leukemogenesis and immune dysfunction remains poorly defined. Here, we identified fibroblast‑derived fibroblast growth factor 18 (FGF18) as a novel stromal cytokine that reprograms leukemia-immune interactions. Single-cell RNA sequencing of the bone marrow (BM) niche during acute myeloid leukemia (AML) revealed the upregulation of Fgf18 in stromal fibroblasts. Administration of recombinant FGF18 accelerated AML progression, whereas fibroblast-specific Fgf18 depletion markedly delayed disease development and improved the survival of mice. We performed a pooled CRISPR-Cas9 screen in AML cells and identified FGFR3 signaling as a critical mediator of leukemic fitness in the FGF18‑rich microenvironment. Genetic loss of Fgfr3 in AML cells recapitulated the effects of FGF18 deficiency and limited leukemic expansion in vivo. Mechanistically, FGF18 binds to its receptor, FGFR3, on AML cells, activating the AKT-mTOR signaling pathway and inducing interleukin (IL)-6 production. IL‑6 acts autocrinely to reinforce leukemic signaling and paracrinely to activate fibroblast JAK-STAT3 signaling, thereby amplifying stromal fibroblast FGF18 expression and forming a feed‑forward loop that suppresses CD8⁺ T‑cell effector function and weakens anti‑leukemic immunity. Clinically, elevated FGF18 expression correlates with poor prognosis in AML patients. To therapeutically target this malignant crosstalk, we generated an FGF18‑neutralizing antibody that disrupted the stromal-leukemia feedback loop, restored CD8⁺ T cell effector function, and synergized with anti-PD-1 therapy to elicit durable anti‑leukemic immunity in vivo. Collectively, these findings identify FGF18-dependent stromal-leukemia crosstalk that drives AML progression and immune dysfunction, highlighting FGF18 neutralization as a potential therapeutic strategy. - Source: PubMed
Publication date: 2026/06/26
Zhang WujuYe ZhixinZhou XuanXiong PengfeiPan YatingQiu JieleiLi MeifangShen JinglingLi YuhuaLu 姚Chen YiranBai XiaochunXie Xiaoling - The purpose of this work was to examine the function of fibroblast growth factor 18 (FGF18) in rat myocardial ischemia-reperfusion injury (MIRI) and elucidate its relationship to mitochondrial function through the Sirtuin 1/peroxisome proliferator-activated receptor gamma coactivator 1 (SIRT1/PGC-1α) pathway. To evaluate myocardial infarct size, pathological alterations, cardiomyocyte injury, mitochondrial state, oxidative stress, and SIRT1/PGC-1α protein expression, FGF18-knockdown and FGF18-overexpression rat MIRI models were created. H9c2 cardiomyocytes were used to create an hypoxia-reoxygenation (H/R) model, and FGF18-overexpressing H9c2 cells were given the SIRT1 inhibitor EX-527. We detected the effects of FGF18-mediated regulation of the SIRT1/PGC-1α pathway on H/R-induced alterations in H9c2 cells, including cell viability, mitochondrial reactive oxygen species (ROS) production, mitochondrial membrane potential, apoptotic rate, and the protein expression of FGF18, SIRT1, PGC-1α, and mitofusin 1 (Mfn1). Furthermore, we performed a protein immunoprecipitation (IP)-protein acetylation assay to determine whether FGF18 influences the acetylation level of PGC-1α through the regulation of SIRT1. Results showed that FGF18 overexpression upregulated SIRT1/PGC-1α/Mfn1 expression, improved mitochondrial function, reduced oxidative stress, and enhanced H9c2 survival under H/R, while FGF18 knockdown had opposite effects. Moreover, FGF18 overexpression inhibited H/R-induced PGC-1α acetylation, and SIRT1 inhibition abrogated FGF18-mediated protective effects. Collectively, FGF18 attenuates rat myocardial MIRI by alleviating oxidative stress and regulating mitochondrial homeostasis through SIRT1-mediated deacetylation of PGC-1α. - Source: PubMed
Publication date: 2026/06/15
Yang HaijiaoHe GuangleiCui XiaojingLi Fei - Osteoporosis is a prevalent musculoskeletal disorder, rising in incidence and impact as the global population ages. Peak bone mass (PBM), determined by bone mineral density (BMD) during adolescence, is a key determinant of skeletal health and later osteoporosis risk. Exercise enhances BMD, yet its molecular mechanisms remain unclear. This study examined combined exercise effects on bone health in early adult mice using RNA sequencing (RNA-seq) analysis. Nineteen-week-old mice were randomly assigned to control (CON, n=8) or combined exercise (EXE, n=8) groups. The 12-week intervention included aerobic and resistance training, with physical performance tests conducted before and after. Following intervention, tibial bone characteristics were assessed by dual-energy X-ray absorptiometry (DXA) and micro-computed tomography (μCT), while femoral gene expression was analyzed using transcriptomic analysis. EXE mice demonstrated significant increases in grip strength and exhaustion test performance, but not in the rotarod test. Proximal tibial trabecular bone microarchitecture was enhanced in the EXE group, with increased bone volume fraction (BV/TV), trabecular thickness (Tb.Th), and trabecular number (Tb.N), along with a trend toward reduced trabecular separation(Tb.Sp). Transcriptomic analysis revealed 109 upregulated and 551 downregulated differentially expressed genes. Gene ontology analysis highlighted enrichment of terms related to muscle cell differentiation, contraction, and ion regulation. Bone metabolism-related GO Biological Process terms were specifically enriched, with Pax1 and Dcstamp upregulated and Fgf18, Scx, and Scube2 downregulated. KEGG analysis identified eleven significantly enriched pathways, including Calcium signaling, ECM-receptor interaction, and PI3K-Akt signaling. These findings suggest that combined exercise enhances trabecular bone microarchitecture and induces transcriptomic changes involving genes associated with bone development, remodeling, and extracellular matrix organization, providing molecular-level evidence for exercise-induced skeletal adaptation. - Source: PubMed
Publication date: 2026/06/15
Kim JiyeonLee SeungyongCho JinkyungMoon Hyo YoulPark Hee-JungPark Dong-HoKim Changsun