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Calcipotriol inhibits proliferation of human keratinocytes by downregulating STAT1 and STAT3 signaling

Wenli Liang, Zigang Lin, Li Zhang, Xuan Qin, Yuan Zhang, Ledong Sun
DOI: 10.1136/jim-2016-000176 Published 26 January 2017
Wenli Liang
1Nursing School of Guangdong Pharmaceutical University, Guangzhou, China
2Department of Dermatology, Zhujiang Hospital, Southern Medical University, Guangzhou, China
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Zigang Lin
3Department of Dermatology, 421 Hospital of People's Liberation Army, Guangzhou, China
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Li Zhang
2Department of Dermatology, Zhujiang Hospital, Southern Medical University, Guangzhou, China
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Xuan Qin
2Department of Dermatology, Zhujiang Hospital, Southern Medical University, Guangzhou, China
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Yuan Zhang
2Department of Dermatology, Zhujiang Hospital, Southern Medical University, Guangzhou, China
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Ledong Sun
2Department of Dermatology, Zhujiang Hospital, Southern Medical University, Guangzhou, China
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Abstract

Psoriasis is an autoimmune disease, which is characterized by aberrantly high levels of inflammation, but the underlying pathogenic mechanisms are still not fully understood. Signal transducer and activator of transcription 1 (STAT1) and STAT3, and the downstream proteins suppressor of cytokine signaling 1 (SOCS1) and SOCS3, have been implicated in psoriasis disease progression. Calcipotriol, a synthetic derivative of vitamin D, has been used clinically to treat psoriasis, but the mechanism of action that underlies the beneficial effects of calcipotriol is still being explored. The objective of this study was to determine whether STAT1 and STAT3 signaling is involved in calcipotriol treatment. Using an in vitro immortal human keratinocyte cell line, HaCaT cells, as a psoriasis model, we examined the molecular signaling induced by calcipotriol treatment. We found that calcipotriol treatment or silencing of either STAT1 or STAT3 inhibited proliferation of HaCaT cells. Calcipotriol downregulated the expression of STAT1 and STAT3 at the messenger RNA (mRNA) and protein levels. The levels of phosphorylated STAT1 and STAT3 were also decreased, suggesting calcipotriol treatment inhibited STAT1 and STAT3 activation. Calcipotriol-mediated STAT inhibition was further substantiated by the downregulation of SOCS1 and SOCS3 at the mRNA and protein expression levels. Taken together, our results suggest a novel molecular mechanism for calcipotriol-mediated treatment effects in psoriasis.

Footnotes

  • WL, ZL and LZ contributed equally.

  • Contributors LS designed the study and wrote the protocol. LS, WL and ZL performed research/study. ZL, LZ, XQ and YZ managed the literature searches and analyses. WL and LS wrote the first draft of the manuscript. LS took overall responsibility. All authors have read and approved the final draft of this article.

  • Funding This study was supported by Science and Technology Planning Project of Guangdong Province, China (grant number 2011B031800106) and the Fund of Chinese Medical Society of Dermatology (grant number 2012003).

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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Vol 65 Issue 2 Table of Contents
Journal of Investigative Medicine: 65 (2)
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Calcipotriol inhibits proliferation of human keratinocytes by downregulating STAT1 and STAT3 signaling
Wenli Liang, Zigang Lin, Li Zhang, Xuan Qin, Yuan Zhang, Ledong Sun
Journal of Investigative Medicine Feb 2017, 65 (2) 376-381; DOI: 10.1136/jim-2016-000176

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Calcipotriol inhibits proliferation of human keratinocytes by downregulating STAT1 and STAT3 signaling
Wenli Liang, Zigang Lin, Li Zhang, Xuan Qin, Yuan Zhang, Ledong Sun
Journal of Investigative Medicine Feb 2017, 65 (2) 376-381; DOI: 10.1136/jim-2016-000176
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Calcipotriol inhibits proliferation of human keratinocytes by downregulating STAT1 and STAT3 signaling
Wenli Liang, Zigang Lin, Li Zhang, Xuan Qin, Yuan Zhang, Ledong Sun
Journal of Investigative Medicine Feb 2017, 65 (2) 376-381; DOI: 10.1136/jim-2016-000176
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