4.7 Article

Transcriptome analysis of human dermal fibroblasts following red light phototherapy

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SCIENTIFIC REPORTS
卷 11, 期 1, 页码 -

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NATURE RESEARCH
DOI: 10.1038/s41598-021-86623-2

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  1. National Institute of General Medical Sciences of the NIH [K23GM117309]
  2. National Cancer Institute of the NIH [P30CA093373]
  3. UC Davis Department of Dermatology Funding

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Red light phototherapy can improve skin fibrosis by regulating extracellular matrices, proliferation, and cellular responses to oxygen-containing compounds. The study found that red light therapy may have anti-fibrotic effects by increasing the expression of MMP1 and PRSS35.
Fibrosis occurs when collagen deposition and fibroblast proliferation replace healthy tissue. Red light (RL) may improve skin fibrosis via photobiomodulation, the process by which photosensitive chromophores in cells absorb visible or near-infrared light and undergo photophysical reactions. Our previous research demonstrated that high fluence RL reduces fibroblast proliferation, collagen deposition, and migration. Despite the identification of several cellular mechanisms underpinning RL phototherapy, little is known about the transcriptional changes that lead to anti-fibrotic cellular responses. Herein, RNA sequencing was performed on human dermal fibroblasts treated with RL phototherapy. Pathway enrichment and transcription factor analysis revealed regulation of extracellular matrices, proliferation, and cellular responses to oxygen-containing compounds following RL phototherapy. Specifically, RL phototherapy increased the expression of MMP1, which codes for matrix metalloproteinase-1 (MMP-1) and is responsible for remodeling extracellular collagen. Differential regulation of MMP1 was confirmed with RT-qPCR and ELISA. Additionally, RL upregulated PRSS35, which has not been previously associated with skin activity, but has known anti-fibrotic functions. Our results suggest that RL may benefit patients by altering fibrotic gene expression.

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