Редактирование: FGF7

Fibroblast growth factor 7 precursor (FGF-7) (Heparin-binding growth factor 7) (HBGF-7) (Keratinocyte growth factor) [KGF]

==Publications==

{{medline-entry
|title=Prostatic microenvironment in senescence: fibroblastic growth factors × hormonal imbalance.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24362909
|abstract=The aim was to characterize and correlate steroid hormone receptors with the [[FGF2]], [[FGF7]] and [[FGF8]] reactivities in the prostatic epithelium and stroma in senile rats. Fifty male senile rats and 10 young male rats were divided into the young (YNG), the senile groups (SE), the castrated group (CAS), the estrogen-deficient group (ED), the castrated   estrogen group (CASE), and the estrogen-deficient   androgen group (EDTEST). The ventral prostate was submitted to immunohistochemical and Western blotting analyses. The results showed decreased [[AR]] and ERβ levels and increased ERα in the senile animals in relation to YNG group. Increased ERα and ERβ reactivities presenting differential localization were characterized in the CASE group compared to the CAS group. Increased [[FGF2]] level was observed in the stroma of the CAS and ED groups in relation to the SE group and in the epithelium of the ED group in relation to the other groups. Increased and differential immunolocalization of [[FGF7]] levels were observed in the CAS, ED and CASE groups. The [[FGF8]] levels showed differential localization in the CAS and ED groups compared to the senile group. The intense hormone ablation was favorable to the autocrine signaling of [[FGF2]] and [[FGF8]]. [[FGF7]] could be activated in the androgen-independent via considering the increased [[FGF7]] in the castrated rats. We concluded that hormone ablation in senescence was favorable to activation or/and to fibroblast signaling in the prostatic microenvironment.
|mesh-terms=* Aging
* Animals
* Cellular Microenvironment
* Estrogens
* Fibroblast Growth Factors
* Gonadal Steroid Hormones
* Male
* Orchiectomy
* Prostate
* Rats
* Rats, Sprague-Dawley
* Receptors, Androgen
* Receptors, Estrogen
* Testosterone

|full-text-url=https://sci-hub.do/10.1007/s00418-013-1173-y
}}
{{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=Negative autoregulation of fibroblast growth factor receptor 2 expression characterizing cranial development in cases of Apert (P253R mutation) and Pfeiffer (C278F mutation) syndromes and suggesting a basis for differences in their cranial phenotypes.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/11596961
|abstract=Heterogeneous mutations in the fibroblast growth factor receptor 2 gene ([[FGFR2]]) cause a range of craniosynostosis syndromes. The specificity of the Apert syndrome-affected cranial phenotype reflects its narrow mutational range: 98% of cases of Apert syndrome result from an Ser252Trp or Pro253Arg mutation in the immunoglobulin-like (Ig)IIIa extracellular subdomain of [[FGFR2]]. In contrast, a broad range of mutations throughout the extracellular domain of [[FGFR2]] causes the overlapping cranial phenotypes of Pfeiffer and Crouzon syndromes and related craniofacial dysostoses. In this paper the expression of [[FGFR1]], the IgIIIa/c and IgIIIa/b isoforms of [[FGFR2]], and [[FGFR3]] is investigated in Apert syndrome (P253R mutation)- and Pfeiffer syndrome (C278F mutation)-affected fetal cranial tissue and is contrasted with healthy human control tissues. Both [[FGFR1]] and [[FGFR3]] are normally expressed in the differentiated osteoblasts of the periosteum and osteoid, in domains overlapped by that of [[FGFR2]], which widely include preosseous cranial mesenchyme. Expression of [[FGFR2]], however, is restricted to domains of advanced osseous differentiation in both Apert syndrome- and Pfeiffer syndrome-affected cranial skeletogenesis in the presence of fibroblast growth factor (FGF)2, but not in the presence of [[FGF4]] or [[FGF7]]. Whereas expression of the [[FGFR2]]-IgIIIa/b (KGFR) isoform is restricted in normal human cranial osteogenesis, there is preliminary evidence that KGFR is ectopically expressed in Pfeiffer syndrome-affected cranial osteogenesis. Contraction of the [[FGFR2]]-IgIIIa/c (BEK) expression domain in cases of Apert syndrome- and Pfeiffer syndrome-affected fetal cranial ossification suggests that the mutant activation of this receptor, by ligand-dependent or ligand-independent means, results in negative autoregulation. This phenomenon, resulting from different mechanisms in the two syndromes, offers a model by which to explain differences in their cranial phenotypes.
|mesh-terms=* Acrocephalosyndactylia
* Aging
* Embryonic and Fetal Development
* Fetus
* Homeostasis
* Humans
* Infant
* Mutation
* Osteogenesis
* Phenotype
* Receptor Protein-Tyrosine Kinases
* Receptor, Fibroblast Growth Factor, Type 1
* Receptor, Fibroblast Growth Factor, Type 2
* Receptors, Fibroblast Growth Factor
* Skull

|full-text-url=https://sci-hub.do/10.3171/jns.2001.95.4.0660
}}
{{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
}}