Abstract:
:Fibroblast migration is a central process in skin wound healing, which requires the coordination of several types of growth factors. bFGF, a well-known fibroblast growth factor (FGF), is able to accelerate fibroblast migration; however, the underlying mechanism of bFGF regulation fibroblast migration remains unclear. Through the RNA-seq analysis, we had identified that the hedgehog (Hh) canonical pathway genes including Smoothened (Smo) and Gli1, were regulated by bFGF. Further analysis revealed that activation of the Hh pathway via up-regulation of Smo promoted fibroblast migration, invasion, and skin wound healing, but which significantly reduced by GANT61, a selective antagonist of Gli1/Gli2. Western blot analyses and siRNA transfection assays demonstrated that Smo acted upstream of phosphoinositide 3-kinase (PI3K)-c-Jun N-terminal kinase (JNK)-β-catenin to promote cell migration. Moreover, RNA-seq and qRT-PCR analyses revealed that Hh pathway genes including Smo and Gli1 were under control of β-catenin, suggesting that β-catenin turn feedback activates Hh signaling. Taken together, our analyses identified a new bFGF-regulating mechanism by which Hh signaling regulates human fibroblast migration, and the data presented here opens a new avenue for the wound healing therapy.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Zhu ZX,Sun CC,Ting Zhu Y,Wang Y,Wang T,Chi LS,Cai WH,Zheng JY,Zhou X,Cong WT,Li XK,Jin LTdoi
10.1016/j.yexcr.2017.03.054subject
Has Abstractpub_date
2017-06-15 00:00:00pages
83-94issue
2eissn
0014-4827issn
1090-2422pii
S0014-4827(17)30181-7journal_volume
355pub_type
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