Abstract
The skin-associated chemokine CCL27 and its receptor CCR10 mediate the immune response of skin-homing T cells. The CCL27 secreted from keratinocytes was reportedly involved in inflammatory skin diseases such as atopic dermatitis, contact dermatitis, and psoriasis. However, whether ionizing radiation increases the levels of CCL27 secretion still remains unclear. In HaCaT cells, a human keratinocyte cell line, CCL27 secretion was markedly increased after X-ray irradiation. We further found that irradiation boosted the generation of reactive oxygen species (ROS), which was concomitant with the release of tumor necrosis factor-alpha (TNF-α). Moreover, alteration of ROS in irradiated HaCaT cells correlated with TNF-α secretion, indicating a positive loop of TNF-α secretion and ROS generation. This positive loop regulated the secretion of CCL27 from irradiated cells. We therefore concluded that the cross talk between TNF-α and ROS after keratinocytes was exposed to radiation, triggered CCL27 secretion for subsequent inflammation response.
| Original language | English (US) |
|---|---|
| Article number | e21868 |
| Journal | Journal of Biochemical and Molecular Toxicology |
| Volume | 31 |
| Issue number | 3 |
| DOIs | |
| State | Published - Mar 1 2017 |
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All Science Journal Classification (ASJC) codes
- Biochemistry
- Molecular Medicine
- Molecular Biology
- Toxicology
- Health, Toxicology and Mutagenesis
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Ionizing radiation promotes CCL27 secretion from keratinocytes through the cross talk between TNF-α and ROS. / Zhang, Qian; Zhu, Linlin; Wang, Gang; Zhao, Ye; Xiong, Na; Bao, Hegang; Jin, Wensen.
In: Journal of Biochemical and Molecular Toxicology, Vol. 31, No. 3, e21868, 01.03.2017.Research output: Contribution to journal › Article
TY - JOUR
T1 - Ionizing radiation promotes CCL27 secretion from keratinocytes through the cross talk between TNF-α and ROS
AU - Zhang, Qian
AU - Zhu, Linlin
AU - Wang, Gang
AU - Zhao, Ye
AU - Xiong, Na
AU - Bao, Hegang
AU - Jin, Wensen
PY - 2017/3/1
Y1 - 2017/3/1
N2 - The skin-associated chemokine CCL27 and its receptor CCR10 mediate the immune response of skin-homing T cells. The CCL27 secreted from keratinocytes was reportedly involved in inflammatory skin diseases such as atopic dermatitis, contact dermatitis, and psoriasis. However, whether ionizing radiation increases the levels of CCL27 secretion still remains unclear. In HaCaT cells, a human keratinocyte cell line, CCL27 secretion was markedly increased after X-ray irradiation. We further found that irradiation boosted the generation of reactive oxygen species (ROS), which was concomitant with the release of tumor necrosis factor-alpha (TNF-α). Moreover, alteration of ROS in irradiated HaCaT cells correlated with TNF-α secretion, indicating a positive loop of TNF-α secretion and ROS generation. This positive loop regulated the secretion of CCL27 from irradiated cells. We therefore concluded that the cross talk between TNF-α and ROS after keratinocytes was exposed to radiation, triggered CCL27 secretion for subsequent inflammation response.
AB - The skin-associated chemokine CCL27 and its receptor CCR10 mediate the immune response of skin-homing T cells. The CCL27 secreted from keratinocytes was reportedly involved in inflammatory skin diseases such as atopic dermatitis, contact dermatitis, and psoriasis. However, whether ionizing radiation increases the levels of CCL27 secretion still remains unclear. In HaCaT cells, a human keratinocyte cell line, CCL27 secretion was markedly increased after X-ray irradiation. We further found that irradiation boosted the generation of reactive oxygen species (ROS), which was concomitant with the release of tumor necrosis factor-alpha (TNF-α). Moreover, alteration of ROS in irradiated HaCaT cells correlated with TNF-α secretion, indicating a positive loop of TNF-α secretion and ROS generation. This positive loop regulated the secretion of CCL27 from irradiated cells. We therefore concluded that the cross talk between TNF-α and ROS after keratinocytes was exposed to radiation, triggered CCL27 secretion for subsequent inflammation response.
UR - http://www.scopus.com/inward/record.url?scp=85005950224&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85005950224&partnerID=8YFLogxK
U2 - 10.1002/jbt.21868
DO - 10.1002/jbt.21868
M3 - Article
C2 - 27879026
AN - SCOPUS:85005950224
VL - 31
JO - Journal of Biochemical and Molecular Toxicology
JF - Journal of Biochemical and Molecular Toxicology
SN - 1095-6670
IS - 3
M1 - e21868
ER -