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Updated: May 16, 2026

Isolation of Papillary and Reticular Fibroblasts from Human Skin by Fluorescence-activated Cell Sorting
Published on: May 7, 2019
Differentiation of rat dermal papilla cells into fibroblast-like cells induced by transforming growth factor β1
Li Hou-dong1, Shu Bin, Xu Ying-bin
1Department of Burns,Yichang Hospital of Traditional Chinese Medicine, Clinical College of Traditional Chinese Medicine of China, Three Gorges Univerity, Yichang.
Background:
The origin of wound-healing fibroblasts is still debated. Dermal papilla cells (DPCs), which are an important population of stem cells for the regeneration of hair follicles, play a considerable role in cutaneous wound healing. Based on the plasticity of DPCs in wound healing, we hypothesized that DPCs may contribute to the fibroblast population of wound repair.
Objective:
To explore the possibility of differentiation of DPCs into fibroblasts induced by transforming growth factor β1 (TGF-β1).
Methods:
The fourth passage DPCs were treated with TGF-β1 (10 ng/mL) for 4 days, and a series of methods was used to observe morphologic changes under an inverted phase contrast microscope, to validate the messenger ribonucleic acid expression change in α-smooth muscle actin (α-SMA) and vimentin by quantitative real-time reverse transcriptase polymerase chain reaction (QRT-PCR), to analyze the expression of α-SMA and vimentin protein by flow cytometry, and to semiquantitatively measure the expression of fibroblast-specific protein 1 (FSP1) by Western blot.
Results:
DPCs treated with TGF-β1 presented fibroblast-like changes in morphology and immunocytochemistry. The effects of TGF-β1 on α-SMA and vimentin in DPCs were detected on both the transcriptional and the posttranscriptional levels. The results showed that TGF-β1 significantly downregulated α-SMA expression and enhanced the expression of vimentin at all times tested. Further study revealed that TGF-β1 could gradually promote the expression of FSP1 in a time-dependent manner.
Conclusion:
DPCs experienced the changes in molecular marker expression in response to TGF-β1, which may be a key source of fibroblasts in wound healing.
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