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人真皮成纤维细胞经红光光疗后的转录组分析。

Transcriptome analysis of human dermal fibroblasts following red light phototherapy.

机构信息

Department of Dermatology, University of California at Davis, Sacramento, CA, USA.

Department of Dermatology, SUNY Downstate, Brooklyn, NY, USA.

出版信息

Sci Rep. 2021 Apr 1;11(1):7315. doi: 10.1038/s41598-021-86623-2.

DOI:10.1038/s41598-021-86623-2
PMID:33795767
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8017006/
Abstract

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.

摘要

当胶原蛋白沉积和成纤维细胞增殖取代健康组织时,就会发生纤维化。红光(RL)可以通过光生物调节来改善皮肤纤维化,光生物调节是细胞内光敏感色素吸收可见光或近红外光并发生光物理反应的过程。我们之前的研究表明,高剂量 RL 可减少成纤维细胞增殖、胶原蛋白沉积和迁移。尽管已经确定了几种支持 RL 光疗的细胞机制,但对于导致抗纤维化细胞反应的转录变化知之甚少。在此,对接受 RL 光疗的人真皮成纤维细胞进行了 RNA 测序。通路富集和转录因子分析表明,RL 光疗后细胞对细胞外基质、增殖和含氧化合物的反应受到调节。具体而言,RL 光疗增加了编码基质金属蛋白酶-1(MMP-1)的 MMP1 的表达,该蛋白负责重塑细胞外胶原蛋白。通过 RT-qPCR 和 ELISA 证实了 MMP1 的差异调节。此外,RL 上调了 PRSS35 的表达,PRSS35 以前与皮肤活性无关,但具有已知的抗纤维化功能。我们的研究结果表明,RL 通过改变纤维化基因表达可能有益于患者。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/143e/8017006/777e7af9a5a3/41598_2021_86623_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/143e/8017006/a22b50e43065/41598_2021_86623_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/143e/8017006/1df1a5630c00/41598_2021_86623_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/143e/8017006/777e7af9a5a3/41598_2021_86623_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/143e/8017006/a22b50e43065/41598_2021_86623_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/143e/8017006/1df1a5630c00/41598_2021_86623_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/143e/8017006/777e7af9a5a3/41598_2021_86623_Fig3_HTML.jpg

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