Fibroblast growth factor (FGF)2/basic FGF is a member of the fibroblast growth factor family. Its role in skin tissue healing is well known in the medical community. Still, the function of other FGFs in skin tissues remains unclear. In this recent study, they studied FGF composition patterns in the heart, liver, skin, and kidney tissues. Compared to other tissues, only four FGFs were dominant in the skin.
- FGF2
- FGF7
- FGF10
- FGF21
To discover FGF function in the tissue healing cycle, mice fibroblast cells were treated with FGF2, FGF10, and FGF21, and cell migration was closely watched. The results showed that FGF treatment improved cell migration, which is an essential step in wound healing. Also, FGF therapy improved the activity of c-Jun N-terminal kinase (JNK), which is a crucial regulator of fibroblast cell movement.
How Does It Heal Wounds?
Human genomes contain 23 members of the fibroblast growth factor family, which are necessary for metabolism and growth. FGF21 is the most researched family member and has been most commonly found in the liver early in development. Skin tissue repair needs the assistance of different cell types, including keratinocytes, fibroblasts, endothelial cells, macrophages, and platelets.
Fibroblast cell generation and migration, collagen deposition, and remodeling wound contraction, and angiogenesis are essential steps of tissue repair. Extracellular matrix forms the most significant component of the dermal skin layer; therefore, the repair of ECM is critical to wound healing. Fibroblasts form an essential cell layer that aids in the production and restoration of the ECM, and their proliferation and migration is vital for the formation of granulation tissue and skin repair.
Is FGF Effective at Healing the Skin?
GF2/bFGF is a member of the FGF family, and its effectiveness in the growth of fibroblast cell migration is recognized in the medical community. In the study, it was observed that FGF2, FGF7, 10, and 21 are highly expressed in skin tissue. Previously, the role of FGF21 in glucose homeostasis has been well known, and its generation is started by stress in the liver and heart. However, in the study, FGF21 appearance was shown to be most significant in the skin, where expression was even higher than in the liver.
Even more impressive is that FGF21 was shown to accelerate the migration of mouse fibroblast cells, similar to FGF2. Also, FGF10 was identified as predominant in the skin and even accelerated cell migration. FGF2 has been known to expedite fibroblast cell migration via activation of the phosphoinositide 3-kinase-Ras-related C3 botulinum toxin substrate 1-JNK signaling pathway. Something else discovered in the study was that FGF2, 10, and 21 treatment increased JNK phosphorylation levels. FGF7 has the highest expression of all FGFs in the skin; however, overexpression of FGF7 in fibroblast cells did not alter cell migration speed, implying that FGF7 may have alternative roles in skin tissue.
Numerous FGFs were comparatively highly expressed in the heart, liver, and kidney, implying the potential roles of these FGFs in different tissues. Notably, FGF1 was one of the dominant FGFs in all the tissues tested besides the skin. The findings of the study show that FGF family members FGF2, 10, and 21 coordinate to stimulate the FGF signaling pathway, which is essential in the development of wound repair.
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