Редактирование: FGF10

Fibroblast growth factor 10 precursor (FGF-10) (Keratinocyte growth factor 2)

==Publications==

{{medline-entry
|title=FGFR2IIIb signaling regulates thymic epithelial differentiation.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/17969154
|abstract=Heterogeneous epithelial populations comprising the thymic environment influence early and late stages of T-cell development. The processes that regulate the differentiation of thymic epithelium and that are responsible for this heterogeneity are not well understood, although mesenchymal/epithelial interactions are clearly involved. Here, we show that targeted expression by thymocytes of an fibroblast growth factor receptor-2IIIb (FGFR2IIIb) ligand, [[FGF10]], profoundly alters the differentiation and function of thymic epithelium (TE). Reconstitution of irradiated lck[[FGF10]] mice with normal bone marrow restores normal thymic organization and function, while wild-type mice reconstituted with lck[[FGF10]] bone marrow recapitulates some of the thymic alterations seen in lck[[FGF10]] mice. We also demonstrate that interference with FGFR2IIIb signaling in the thymus with a soluble FGFR2IIIb dominant-negative fusion protein leads to precocious reductions in thymic size and cellularity that resemble age-related thymic involution. These findings indicate that TE compartments are dynamically maintained and that FGF signals are involved in this process.
|mesh-terms=* Aging
* Animals
* Base Sequence
* DNA Primers
* Epithelium
* Fibroblast Growth Factor 10
* Gene Expression Regulation, Developmental
* Gene Targeting
* Humans
* Keratins
* Mice
* Mice, Inbred C57BL
* Mice, Knockout
* Mice, Transgenic
* Phenotype
* Protein Isoforms
* Receptor, Fibroblast Growth Factor, Type 2
* Recombinant Proteins
* Signal Transduction
* T-Lymphocytes
* Thymus Gland

|full-text-url=https://sci-hub.do/10.1002/dvdy.21364
}}
{{medline-entry
|title=Expression of fibroblast growth factors and their receptors during full-thickness skin wound healing in young and aged mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/16079254
|abstract=The highly ordered process of wound healing involves the coordinated regulation of cell proliferation and migration and tissue remodeling, predominantly by polypeptide growth factors. Consequently, the slowing of wound healing that occurs in the aged may be related to changes in the activity of these various regulatory factors. To gain additional insight into these issues, we quantified the absolute copy numbers of mRNAs encoding all the fibroblast growth factors (FGFs), their receptors (FGFRs) and two other growth factors in the dorsal skin of young and aged mice during the healing of full-thickness skin excisional wounds. In young adult mice (8 weeks old), [[FGF7]], [[FGF10]] and [[FGF22]] mRNAs were all strongly expressed in healthy skin, and levels of [[FGF7]] and 10 but not 22 increased 2- to 3.5-fold over differing time courses after wounding. The levels of [[FGF9]], 16, 18 and especially 23 mRNAs were moderate or low in healthy skin but increased 2- to 33-fold after wounding. Among the four FGFRs, expression of only [[FGFR1]] mRNA was augmented during wound healing. Expression of transforming growth factor-beta and hepatocyte growth factor was also high in healthy skin and was upregulated during healing. Notably, in aged mice (35 weeks old), where healing proceeded more slowly than in the young, both the basal and wound-induced mRNA expression of most of these genes was reduced. While these results confirm the established notion that [[FGFR2]] IIIB ligands ([[FGF7]] and [[FGF10]]) are important for wound healing, they also suggest that decreased expression of multiple FGF ligands contributes to the slowing of wound healing in aged mice and indicate the potential importance of further study of the involvement of [[FGF9]], 16, 18 and 23 in the wound healing process.
|mesh-terms=* Actins
* Aging
* Animals
* Fibroblast Growth Factors
* Gene Expression
* Glyceraldehyde-3-Phosphate Dehydrogenases
* Hepatocyte Growth Factor
* Male
* Mice
* Mice, Mutant Strains
* RNA, Messenger
* Receptors, Fibroblast Growth Factor
* Skin
* Transforming Growth Factor beta
* Wound Healing

|full-text-url=https://sci-hub.do/10.1677/joe.1.06055
}}
{{medline-entry
|title=Attenuation of FGF signalling in mouse beta-cells leads to diabetes.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/11130726
|abstract=Fibroblast growth factor (FGF) signalling has been implicated in patterning, proliferation and cell differentiation in many organs, including the developing pancreas. Here we show that the FGF receptors (FGFRs) 1 and 2, together with the ligands [[FGF1]], [[FGF2]], [[FGF4]], [[FGF5]], [[FGF7]] and [[[[FGF1]]0]], are expressed in adult mouse beta-cells, indicating that FGF signalling may have a role in differentiated beta-cells. When we perturbed signalling by expressing dominant-negative forms of the receptors, [[FGFR1]]c and FGFR2b, in the pancreas, we found that that mice with attenuated [[FGFR1]]c signalling, but not those with reduced FGFR2b signalling, develop diabetes with age and exhibit a decreased number of beta-cells, impaired expression of glucose transporter 2 and increased proinsulin content in beta-cells owing to impaired expression of prohormone convertases 1/3 and 2. These defects are all characteristic of patients with type-2 diabetes. Mutations in the homeobox gene Ipf1/Pdx1 are linked to diabetes in both mouse and human. We also show that Ipf1/Pdx1 is required for the expression of [[FGFR1]] signalling components in beta-cells, indicating that Ipf1/Pdx1 acts upstream of [[FGFR1]] signalling in beta-cells to maintain proper glucose sensing, insulin processing and glucose homeostasis.
|mesh-terms=* Aging
* Animals
* Blood Glucose
* Diabetes Mellitus, Experimental
* Diabetes Mellitus, Type 2
* Fibroblast Growth Factors
* Glucose Transporter Type 1
* Glucose Transporter Type 2
* Homeodomain Proteins
* Humans
* Insulin
* Islets of Langerhans
* Mice
* Mice, Transgenic
* Monosaccharide Transport Proteins
* Pancreas
* Receptor Protein-Tyrosine Kinases
* Receptor, Fibroblast Growth Factor, Type 1
* Receptor, Fibroblast Growth Factor, Type 2
* Receptors, Fibroblast Growth Factor
* Signal Transduction
* Trans-Activators

|full-text-url=https://sci-hub.do/10.1038/35048589
}}
{{medline-entry
|title=Prostatic growth and development are regulated by [[FGF10]].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/10409514
|abstract=We have examined the role of Fibroblast Growth Factor 10 ([[FGF10]]) during the growth and development of the rat ventral prostate (VP) and seminal vesicle (SV). [[FGF10]] transcripts were abundant at the earliest stages of organ formation and during neonatal organ growth, but were low or absent in growth-quiescent adult organs. In both the VP and SV, [[FGF10]] transcripts were expressed only in a subset of mesenchymal cells and in a pattern consistent with a role as a paracrine epithelial regulator. In the neonatal VP, [[FGF10]] mRNA was expressed initially in mesenchymal cells peripheral to the peri-urethral mesenchyme and distal to the elongating prostatic epithelial buds. At later stages, mesenchymal cells surrounding the epithelial buds also expressed [[FGF10]] transcripts. During induction of the SV, [[FGF10]] mRNA was present in mesenchyme surrounding the lower Wolffian ducts and, at later stages, [[FGF10]] transcripts became restricted to mesenchymal cells subadjacent to the serosa. We investigated whether the [[FGF10]] gene might be regulated by androgens by analysing the levels of [[FGF10]] transcripts in SV and VP organs grown in serum-free organ culture. While [[FGF10]] transcript levels increased after treatment with testosterone in the SV (but not VP), these changes were not sensitive to anti-androgen treatment, and thus it is likely that [[FGF10]] mRNA was not directly regulated by testosterone. Also, [[FGF10]] mRNA was observed in the embryonic female reproductive tract in a position analogous to that of the ventral prostate in males suggesting that [[FGF10]] is not regulated by androgens in vivo. Recombinant [[FGF10]] protein specifically stimulated growth of Dunning epithelial and BPH1 prostatic epithelial cell lines, but had no effect on growth of Dunning stromal cells or primary SV mesenchyme. Furthermore, [[FGF10]] protein stimulated the development of ventral prostate and seminal vesicle organ rudiments in serum-free organ culture. When both [[FGF10]] and testosterone were added to organs in vitro, there was no synergistic induction of development. Additionally, development induced by [[FGF10]] was not inhibited by the addition of the anti-androgen Cyproterone Acetate demonstrating that the effects of [[FGF10]] were not mediated by the androgen receptor. Taken together, our experiments suggest that [[FGF10]] functions as a mesenchymal paracrine regulator of epithelial growth in the prostate and seminal vesicle and that the [[FGF10]] gene is not regulated by androgens
|mesh-terms=* Aging
* Animals
* Animals, Newborn
* Cell Division
* Embryonic and Fetal Development
* Epithelial Cells
* Female
* Fibroblast Growth Factor 10
* Fibroblast Growth Factors
* Gene Expression Regulation, Developmental
* Male
* Organ Culture Techniques
* Organ Specificity
* Prostate
* RNA, Messenger
* Rats
* Rats, Inbred F344
* Recombinant Proteins
* Seminal Vesicles
* Transcription, Genetic


}}