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Gene expression profiling reveals aryl hydrocarbon receptor as a possible target for photobiomodulation when using blue light

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ABSTRACT

Photobiomodulation (PBM) with blue light induces a biphasic dose response curve in proliferation of immortalized human keratinocytes (HaCaT), with a maximum anti-proliferative effect reached with 30min (41.4 J/cm2). The aim of this study was to test the photobiomodulatory effect of 41.4 J/cm2 blue light irradiation on ROS production, apoptosis and gene expression at different time points after irradiation of HaCaT cells in vitro and assess its safety. ROS concentration was increased 30 min after irradiation. However, already 1 h after irradiation, cells were able to reduce ROS and balance the concentration to a normal level. The sudden increase in ROS did not damage the cells, which was demonstrated with FACS analysis where HaCaT cells did not show any sign of apoptosis after blue light irradiation. Furthermore, a time course could be seen in gene expression analysis after blue light, with an early response of stimulated genes already 1 h after blue light irradiation, leading to the discovery of the aryl hydrocarbon receptor as possible target for blue light irradiation.

No MeSH data available.


Gene set enrichment analysis-time course of the Aryl Hydrocarbon Receptor (AHR) signaling pathway.
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f6: Gene set enrichment analysis-time course of the Aryl Hydrocarbon Receptor (AHR) signaling pathway.

Mentions: CYP1A1 and CYP1B1 were both highly upregulated for all three harvesting time points leading to the identification of a possible functionality of their transcription factor aryl hydrocarbon receptor (AHR) after blue light irradiation. Tryptophan metabolism and chemical carcinogenesis are both pathways containing significantly upregulated genes and are connected to AHR. As KEGG does not provide an AHR pathway was designed (Fig. 5) using a literature search containing inter alia the “AHR battery genes” CYP1A1, CYP1A2, CYP1B1, aldehyde dehydrogenase 3 family member a1 (ALDH3A1), NAD(P)H quinone oxidoreductase 1 (NQO1), UDP glucuronosyltransferase 1 family, polypeptide A (UGT1A), glutathione S-transferase 1 (GSTA1) and genes encoding AHR and its contributors aryl hydrocarbon receptor nuclear translocator (ARNT) and aryl hydrocarbon receptor repressor (AHRR). Additionally, genes deregulated downstream after AHR activation like cyclin-dependent kinase inhibitor 1B (CDKN1B, also KIP1), nuclear factor erythroid 2 like 2 (Nrf2, also NFE2L2) and tumor necrosis factor (TNF-a) receptor-associated protein (TRADD) are depicted. The AHR signaling pathway (Fig. 6) is upregulated for all three time points with p = 0.3300 after 1 h, p < 0.0001 after 3 h and p < 0.0001 24 h after blue light irradiation. The time course of gene expression analysis for these mentioned genes is illustrated in Fig. 7 to help describing that AHR is a possible target for blue light irradiation as explained in the discussion.


Gene expression profiling reveals aryl hydrocarbon receptor as a possible target for photobiomodulation when using blue light
Gene set enrichment analysis-time course of the Aryl Hydrocarbon Receptor (AHR) signaling pathway.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037386&req=5

f6: Gene set enrichment analysis-time course of the Aryl Hydrocarbon Receptor (AHR) signaling pathway.
Mentions: CYP1A1 and CYP1B1 were both highly upregulated for all three harvesting time points leading to the identification of a possible functionality of their transcription factor aryl hydrocarbon receptor (AHR) after blue light irradiation. Tryptophan metabolism and chemical carcinogenesis are both pathways containing significantly upregulated genes and are connected to AHR. As KEGG does not provide an AHR pathway was designed (Fig. 5) using a literature search containing inter alia the “AHR battery genes” CYP1A1, CYP1A2, CYP1B1, aldehyde dehydrogenase 3 family member a1 (ALDH3A1), NAD(P)H quinone oxidoreductase 1 (NQO1), UDP glucuronosyltransferase 1 family, polypeptide A (UGT1A), glutathione S-transferase 1 (GSTA1) and genes encoding AHR and its contributors aryl hydrocarbon receptor nuclear translocator (ARNT) and aryl hydrocarbon receptor repressor (AHRR). Additionally, genes deregulated downstream after AHR activation like cyclin-dependent kinase inhibitor 1B (CDKN1B, also KIP1), nuclear factor erythroid 2 like 2 (Nrf2, also NFE2L2) and tumor necrosis factor (TNF-a) receptor-associated protein (TRADD) are depicted. The AHR signaling pathway (Fig. 6) is upregulated for all three time points with p = 0.3300 after 1 h, p < 0.0001 after 3 h and p < 0.0001 24 h after blue light irradiation. The time course of gene expression analysis for these mentioned genes is illustrated in Fig. 7 to help describing that AHR is a possible target for blue light irradiation as explained in the discussion.

View Article: PubMed Central - PubMed

ABSTRACT

Photobiomodulation (PBM) with blue light induces a biphasic dose response curve in proliferation of immortalized human keratinocytes (HaCaT), with a maximum anti-proliferative effect reached with 30min (41.4&thinsp;J/cm2). The aim of this study was to test the photobiomodulatory effect of 41.4&thinsp;J/cm2 blue light irradiation on ROS production, apoptosis and gene expression at different time points after irradiation of HaCaT cells in vitro and assess its safety. ROS concentration was increased 30&thinsp;min after irradiation. However, already 1&thinsp;h after irradiation, cells were able to reduce ROS and balance the concentration to a normal level. The sudden increase in ROS did not damage the cells, which was demonstrated with FACS analysis where HaCaT cells did not show any sign of apoptosis after blue light irradiation. Furthermore, a time course could be seen in gene expression analysis after blue light, with an early response of stimulated genes already 1&thinsp;h after blue light irradiation, leading to the discovery of the aryl hydrocarbon receptor as possible target for blue light irradiation.

No MeSH data available.