Cooperation of TGF‐β and FGF signalling pathways in skin development

Abstract

The skin is a multi‐layered structure composed of the epidermis, dermis and hypodermis. The epidermis originates entirely from the ectoderm, whereas the dermis originates from various germ layers depending on its anatomical location; thus, there are different developmental patterns of the skin. Although the regulatory mechanisms of epidermal formation are well understood, mechanisms regulating dermis development are not clear owing to the complex origin. It has been shown that several morphogenetic pathways regulate dermis development. Of these, transforming growth factor‐β (TGF‐β) and fibroblast growth factor (FGF) signalling pathways are the main modulators regulating skin cell induction, fate decision, migration and differentiation. Recently, the successful generation of human skin by modulating TGF‐β and FGF signals further demonstrated the irreplaceable roles of these pathways in skin regeneration. This review provides evidence of the role of TGF‐β and FGF signalling pathways in the development of different skin layers, especially the disparate dermis of different body regions. This review also provides new perspectives on the distinct developmental patterns of skin and explores new ideas for clinical applications in the future.

Insights on the In Vitro Wound Healing Effects of Sedum telephium L. Leaf Juice

“…In keratinocyte cultures, SED induced the secretion of TGFβ1 and FGF, two growth factors intrinsically connected [42] and dependent by the master TGF signalling [43]. Noteworthy, the upreguation of TGFβ1 and FGF is a pivotal mechanism also displayed by the well-known aloe gel (Aloe vera (L).…”

Signalling interaction between β‐catenin and other signalling molecules during osteoarthritis development

“…TGF‐β has been shown to be critical for chondrocyte proliferation and extracellular matrix protein synthesis and release. 67 , 68 In our previous study, we found that TGF‐β signalling play an essential role in OA pathogenesis. 69 We have generated chondrocyte‐specific Tgfbr2 conditional knockout mice ( Tgfbr2 Col2ER ).…”