Oncotarget

Research Papers:

Overexpression and potential roles of NRIP1 in psoriasis

Chao Luan, Xu Chen, Yu Hu, Zhimin Hao, Jared M. Osland, Xundi Chen, Skyler D. Gerber, Min Chen _, Heng Gu and Rong Yuan

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Oncotarget. 2016; 7:74236-74246. https://doi.org/10.18632/oncotarget.12371

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Abstract

Chao Luan1,2, Xu Chen1, Yu Hu1, Zhimin Hao1, Jared M. Osland2, Xundi Chen2,3, Skyler D. Gerber2,3, Min Chen1, Heng Gu1, Rong Yuan2

1Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing, Jiangsu, China

2Department of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL, USA

3Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine, Springfield, IL, USA

Correspondence to:

Min Chen, email: [email protected]

Heng Gu, email: [email protected]

Rong Yuan, email: [email protected]

Keywords: NRIP1, psoriasis, skin, T cells, animal model

Received: July 26, 2016     Accepted: September 22, 2016     Published: September 30, 2016

ABSTRACT

Nuclear receptor interacting protein 1 (NRIP1, also known as RIP140) is a co-regulator for various transcriptional factors and nuclear receptors, and has been shown to take part in many biological and pathological processes, such as regulating mammary gland development and inflammatory response.

The aim of this study is to investigate the expression of NRIP1 and to explore its roles in the pathogenesis of psoriasis. Thirty active psoriasis patients and 16 healthy volunteers were enrolled for this study. qRT-PCR analyses found that both NRIP1 and RelA/p65 were elevated in psoriatic lesions compared to psoriatic non-lesions and normal controls, and also overexpressed in peripheral blood mononuclear cell (PBMCs) of psoriasis patients. Suppression of NRIP1 in HaCaT cells could significantly inhibit cell growth and induce apoptosis, and the suppression of NRIP1 in CD4+ T cells isolated from psoriasis patients could downregulate the expression of RelA/p65 and decrease the secretion of IL-17. Furthermore, in Nrip1 knockout mice, IMQ-induced inflammation of skin was delayed and the RelA/p65 expression in lesions was reduced. In conclusion, our data suggests that NRIP1 is overexpressed both in skin and PBMCs of psoriasis patients and may be involved in the abnormal proliferation and apoptosis of keratinocytes, as well as the immune reaction through the regulation of RelA/p65. Therefore, NRIP1 may be a potential therapeutic target for psoriasis.


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