Publication: Reduction of PGRN increased fibrosis during skin wound healing in mice
Authors
Li, Shan-shan ; Zhang, Mei Xiang ; Wang, Yue ; Wang, Wei ; Zhao, Chun Ming ; Sun, Xiao Ming ; Dong, Guo Kai ; Li, Zhou Ru ; Yin, Wen Jiang ; Zhu, Bo ; Cai, Hong Xing
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Publisher
Universidad de Murcia. Departamento de Biología Celular e Histología
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DOI
DOI: 10.14670/HH-18-076
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info:eu-repo/semantics/article
Description
Abstract
Progranulin (PGRN) is a multi-functional
growth factor known to be involved in regulating of
development, cell cycle progression, cell motility,
tumorigenesis and angiogenesis. Research has revealed
that PGRN is a crucial mediator of skin wound healing.
Nonetheless, the role of PGRN in the fibrosis process of
cutaneous wound healing has not been identified. In the
present study, mice with excisional wounds were treated
with si-m-PGRN or physiological saline. We observed
the expression of PGRN in intact and post-injury skin by
immunohistochemistry. Tissue sections of skin around
the wound were performed by hematoxylin and eosin
and masson's trichrome staining. After PGRN
knockdown by siRNA, the expression of PGRN,
collagen I (Col I), small mothers against decapentaplegic
homolog 3 (Smad3), phosphorylated Smad3 (P-Smad3),
transforming growth factor (TGF)-β1 and TGF-β
receptor I (TβRI) were detected by real-time reverse
transcription polymerase chain reaction (RT-qPCR) or
Western blot. PGRN mRNA and protein expressions
were increased after insult and remained above that of
intact skin through day 20. Down-regulation of PGRN
augmented fibrosis area, skin thickness and the
expression of Col I. In addition, reduction of PGRN
considerably increased the expression of TGF-β1, TβRI,
Smad3 and P-Smad3. These results indicate that PGRN
knockdown enhances the fibrosis degree, probably via
the TGF-β/Smad signaling pathway.
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