TY - JOUR
T1 - Transcriptome analysis of human dermal fibroblasts following red light phototherapy
AU - Austin, Evan
AU - Koo, Eugene
AU - Merleev, Alexander
AU - Torre, Denis
AU - Marusina, Alina
AU - Luxardi, Guillaume
AU - Mamalis, Andrew
AU - Isseroff, Roslyn Rivkah
AU - Ma’ayan, Avi
AU - Maverakis, Emanual
AU - Jagdeo, Jared
N1 - Funding Information:
The work presented here was supported by the National Institute of General Medical Sciences of the NIH under Award No. K23GM117309 (Jagdeo), with additional support from the National Cancer Institute of the NIH under Award No. P30CA093373 (Maverakis/UC Davis Cancer Center), and UC Davis Department of Dermatology Funding (Jagdeo).
Funding Information:
The work presented here was supported by the National Institute of General Medical Sciences of the NIH under Award No. K23GM117309 (Jagdeo), with additional support from the National Cancer Institute of the NIH under Award No. P30CA093373 (Maverakis/UC Davis Cancer Center), and UC Davis Department of Dermatology Funding (Jagdeo). The content is solely the responsibility of the authors and does not necessarily represent the views of the US Department of Veterans Affairs or the US government.
Publisher Copyright:
© 2021, The Author(s).
PY - 2021/12
Y1 - 2021/12
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85103807060&partnerID=8YFLogxK
U2 - 10.1038/s41598-021-86623-2
DO - 10.1038/s41598-021-86623-2
M3 - Article
C2 - 33795767
AN - SCOPUS:85103807060
SN - 2045-2322
VL - 11
JO - Scientific Reports
JF - Scientific Reports
IS - 1
M1 - 7315
ER -