Open AccessSonic hedgehog signalling regulates the self‐renewal and proliferation of skin‐derived precursor cells in mice
Author(s) -
Park Sangkyu,
Kim Hyewon,
Kim Kichul,
Roh Sangho
Publication year - 2018
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12500
Subject(s) - cyclopamine , hedgehog signaling pathway , sonic hedgehog , microbiology and biotechnology , biology , apoptosis , hedgehog , signal transduction , stem cell , biochemistry
Objectives The sonic hedgehog (Shh) signalling pathway has an important role in the maintenance of various stem cells and organogenesis during development. However, the effect of Shh in skin‐derived precursors ( SKP s), which have the capacity for multipotency and self‐renewal, is not yet clear. The present study investigated the effects of the Shh signalling pathway on the proliferation and self‐renewal of murine SKP s ( mSKP s). Methods The Shh signalling pathway was activated by treatment with purmorphamine (Shh agonist) or recombinant Shh in mSKP s. Cyclopamine (Shh antagonist) or GANT ‐61 (Gli inhibitor) was used to inhibit the pathway. Western blot, qPCR , and immunofluorescence were used to analyse the expression of genes related to self‐renewal, stemness, epithelial‐mesenchymal transition ( EMT ) and the Shh signalling pathway. In addition, cell proliferation and apoptosis were examined. Results Inhibiting the Shh signalling pathway reduced mSKP proliferation and sphere formation, but increased apoptosis. Activating this signalling pathway produced opposite results. The Shh signalling pathway also controlled the EMT phenotype in mSKP s. Moreover, purmorphamine recovered the self‐renewal and proliferation of aged mSKP s. Conclusion Our results suggest that the Shh signalling pathway has an important role in the proliferation, self‐renewal and apoptosis of mSKP s. These findings also provide a better understanding of the cellular mechanisms underlying SKP self‐renewal and apoptosis that allow more efficient expansion of SKP s.