Ask about this productRelated genes to: FGF10 antibody
- Gene:
- FGF10 NIH gene
- Name:
- fibroblast growth factor 10
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5p12
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-16
- Date modifiied:
- 2016-10-05
Related products to: FGF10 antibody
Related articles to: FGF10 antibody
- The mechanisms by which alveoli form during lung development remain under investigation. The classical model proposes formation through secondary septation, whereas an alternative proposed model suggests that alveoli arise through epithelial budding within preformed mesenchymal stabilizing rings. Regardless of the precise morphogenetic mechanism, alveolar formation depends on coordinated interactions among epithelial progenitor cells, pulmonary endothelial cells, mesenchymal populations, extracellular matrix remodeling, and biomechanical forces. Stereologic imaging supports continued postnatal alveolar formation and the biological plausibility of alveolar regeneration. These observations are relevant to bronchopulmonary dysplasia (BPD), a disorder of interrupted alveolar and pulmonary vascular development after extremely preterm birth. This review integrates competing morphogenetic models with complementary local and systemic therapeutic concepts. Insulin-like growth factor 1 (IGF-1) provides systemic and local support for alveolar, vascular, and multiorgan maturation. In contrast, fibroblast growth factor 10 (FGF10) is a major local morphogen that regulates epithelial branching, alveolar induction, and repair. Physiologic IGF-1 replacement is being evaluated clinically to reduce BPD severity; FGF10-mediated regeneration remains at the preclinical proof-of-concept stage. Together, these pathways illustrate how preserving or resuming developmental signaling may support lifelong lung health after extremely preterm birth. - Source: PubMed
Publication date: 2026/09/18
Warburton DavidMoats RexParton Lance ALaGamma Edmund FNiklas Victoria - Previous studies showed that fortified fibrin hydrogel (Ep-FH), generated by conjugating laminin-1 peptides (A99 and YIGSR) and growth factors (FGF7 and FGF10) to fibrin hydrogels, improves epithelial organization and secretory function in irradiated mouse submandibular glands (SMG). To define the cell type-specific mechanisms underlying these effects, we generated high-resolution spatial transcriptomic profiles using the Xenium Prime Mouse Pan Tissue and Pathways Panel (5,000 genes). Treatment with Ep-FH partially reactivated secretory- and polarity-related genes, shifted stromal and immune transcriptional programs toward the non-irradiated state, and reduced profibrotic signaling. Integrative clustering further showed increased similarity of acinar, stromal, immune, and myoepithelial populations to non-irradiated controls, whereas ductal, endothelial, and glial cells showed limited responses. These findings indicate that Ep-FH partially restores transcriptional programs in selected cell populations, suggesting that further optimization may improve regeneration throughout the irradiated SMG. - Source: PubMed
Publication date: 2026/09/15
Nam KihoonMaienschein-Cline MarkTavares Dos Santos HarimMaslow Frank MOsorio Rodrigo AAndreadis Stelios TBaker Olga J - Thyroid hormones (THs) regulate embryonic growth and tissue remodeling, yet their contribution to avian limb morphogenesis remains incompletely defined. We hypothesized that amiodarone-induced inhibition of TH signaling can disrupt chick hindlimb development by altering key patterning pathways and epithelial-mesenchymal dynamics during early limb bud morphogenesis. Fertilized Rhode Island Red eggs received in ovo air-cell injections of phosphate-buffered saline (control) or amiodarone (1 mM) at embryonic day 0 and were analyzed at days 2, 4, and 10, with some embryos allowed to hatch for phenotypic assessment. Hindlimb development was evaluated using morphological, histological, molecular, cellular, and biochemical approaches, including gene and protein expression analyses, apoptosis and cell-cycle profiling, systems-level pathway analyses, and tissue remodeling endpoints. Amiodarone exposure produced consistent limb deformities at hatching and impaired chondrogenic organization at day 10. Molecular profiling revealed elevated SHH/FGF8/WNT3/HOXA10/CASP3 with concomitant suppression of hindlimb identity and mesenchymal/EMT-associated genes (TBX4, PITX1, FGF10, GLI3, SNAIL, WNT7A). Protein and flow cytometry data supported uncoupling of the AER-mesenchyme axis, increased epithelial CDH1-positive populations with reduced SNAIL, and enhanced cleaved Caspase-3 associated apoptosis, corroborated by expanded Nile Blue staining. Proteomic shifts, reduced acetylcholinesterase activity, and decreased hydroxyproline further suggest disrupted differentiation and matrix maturation. Collectively, these results suggest that intact TH signaling might be essential for coordinating patterning cues, epithelial-mesenchymal balance, cell survival, and extracellular matrix maturation during chick hindlimb development, and that amiodarone exposure is associated with disruption of these integrated developmental programs, which may contribute to the observed structural limb defects. - Source: PubMed
Publication date: 2026/09/07
Vaishnav JuhiBalakrishnan Suresh - The gliding patagium represents a key adaptation for mammalian flight, but its cellular development remains unexplored. Using single-nucleus RNA sequencing of embryonic flying squirrel patagium and dorsal skin, we construct a single-cell atlas of patagium development and identify two distinct fibroblast subpopulations (Fp2 and Fr) highly enriched in the patagium. These fibroblasts are characterized by the patagium upregulation of Wnt5a, Fgf7, and Fgf10, and are associated with patagium morphogenesis through dermal-epidermal putative communication interactions between dermal fibroblasts (Fp2 and Fr) and epithelial basal keratinocytes. Specifically, Fp2 fibroblasts are potentially involved in distal dermal condensation and epithelial thickening together with elevated Wnt5a expression, while both Fp2 and Fr fibroblasts could play a role in epithelial polarization and thickening through Fgf7 and Fgf10, as suggested by ex vivo assays. Our data suggest that gliding patagium development results from the co-option of conserved WNT and FGF signaling pathways within a specialized fibroblast-epithelial context, illustrating how modifications of conserved developmental programs give rise to derived morphological traits. - Source: PubMed
Publication date: 2026/08/04
Lin YouFuHuang ShuangXianChe LiFengZhao HaoZheWang YaJunYang MingFeiAi ChengRuan JueWang XiaoPingYu Li - CRISPR/Cas9-mediated genome editing enables efficient generation of knockout mouse models; however, frameshift mutations do not always result in complete loss of function. The factors influencing functional inactivation following frameshift mutations remain incompletely understood. Here, we tested whether frameshift-dominant targeting of exon 1 is sufficient to generate a null allele of , a gene essential for limb formation. - Source: PubMed
Publication date: 2026/08/01
Lkhagvadorj KhanuiOkamura EiichiMorimura ToshifumiMizuno SeiyaEma Masatsugu