FGF-18, Human Protein
- Known as:
- FGF-18, Human Protein
- Catalog number:
- z03011-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- FGF-18 Human Protein
Related genes to: FGF-18, Human 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, Human Protein
Related articles to: FGF-18, Human Protein
- 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 - The periosteum, a thin membranous tissue covering the external bone surface, is a well-established source of osteogenic activity during bone growth and fracture repair. However, the molecular identity and anatomical niche of its progenitor cells remain incompletely defined. Using single-cell RNA sequencing and RNA in situ hybridization in mouse long bones, we identified that fibroblast growth factor 18 (Fgf18) expression marks a discrete subset of cells within the fibrous layer of the periosteum that co-express genes associated with skeletal stem and progenitor populations. Lineage tracing revealed that Fgf18 cells contribute minimally to cortical bone formation under homeostatic conditions but robustly expand and generate chondrocytes and osteoblasts following injury. Targeted ablation of Fgf18-lineage cells impaired fracture healing, confirming their functional importance. Together, these findings define Fgf18 fibrous periosteal cells as a reserve progenitor population that is activated by injury to regenerate bone. - Source: PubMed
Publication date: 2026/06/11
Ji XingKoehnken Sawall JasminZhang XuejunOrnitz David MLong Fanxin - Oligodendrocytes deposit different amounts of myelin in each neocortical layer, but the regulatory process remains unclear. We present a single-cell map of oligodendrocyte lineage cells purified from different layers of the neocortex across developmental stages. We find that each layer contains a similar compendium of oligodendrocyte classes and differs primarily in the proportions of maturation states, suggesting that oligodendrocyte heterogeneity cannot explain layer-specific myelination. We show that signals from different classes of pyramidal neurons can control oligodendrocyte maturation and the differential distribution of myelin across cortical layers. We generated a ligand-receptor interactome to predict interactions between projection neuron types and oligodendrocyte states, across cortical layers and time, and validated candidates in vivo. We find that neuronal expression of Fgf18, Ncam1, and Rspo3 promotes cortical myelination. This work provides a comprehensive molecular description of oligodendrocyte development in the mouse cortex, pointing to mechanisms whereby neuron-class-linked signals modulate myelin distribution in the neocortex. - Source: PubMed
Publication date: 2026/06/02
Domínguez-Iturza NuriaJokhi VahbizKim KwanhoShetty Ashwin SDi Bella Daniela JPereira Luppi MilagrosYuan WenAbbate CatherineOyler-Castrillo PaulOliver Nalini AVenkat VaishnaviJin XinSimmons SeanLevin Joshua ZBrown Juliana RArlotta Paola - The adhesion of monocytes to vascular endothelial cells constitutes a fundamental early process in atherogenesis. Fibroblast growth factor-18 (FGF-18), known to signal through the fibroblast growth factor receptor 1 (FGFR1), has emerging roles in maintaining vascular homeostasis, but its precise function in endothelial inflammation remains unclear. The protective role of recombinant human FGF-18 (rhFGF-18) against oxidized low-density lipoprotein (ox-LDL)-induced endothelial injury and its mechanism were investigated. We found that ox-LDL downregulated phospho-FGFR1 in human aortic vascular endothelial cells (HAVECs) dose- and time-dependently. rhFGF-18 treatment markedly suppressed ox-LDL-induced upregulation of the scavenger receptor LOX-1 and key pro-inflammatory factors (TNF-α, MCP-1, COX-2, and PGE). Subsequently, rhFGF-18 reduced the expression of adhesion molecules VCAM-1 and ICAM-1, thereby decreasing THP-1 monocyte adhesion to HAVECs. Mechanistic investigations revealed that rhFGF-18 inhibits ox-LDL-induced phosphorylation and nuclear translocation of the transcriptional regulator TRIM28. Importantly, TRIM28 overexpression reversed the anti-inflammatory and anti-adhesive benefits of rhFGF-18. Collectively, this study identifies the FGF-18/TRIM28 axis as a crucial mechanism alleviating endothelial inflammation and monocyte adhesion, highlighting its potential as a therapeutic target for atherosclerosis. - Source: PubMed
Publication date: 2026/03/16
Yuan ChaojuanLiu ZhonglingYe WenjuanDing Hong