title: Overexpression and potential roles of NRIP1 in psoriasis.
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.
authors.affiliation: Jiangsu 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.|Department of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL, USA.
authors.forename: Chao
authors.initials: C
authors.lastname: Luan
authors.affiliation: Jiangsu 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.
authors.forename: Xu
authors.initials: X
authors.lastname: Chen
authors.affiliation: Jiangsu 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.
authors.forename: Yu
authors.initials: Y
authors.lastname: Hu
authors.affiliation: Jiangsu 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.
authors.forename: Zhimin
authors.initials: Z
authors.lastname: Hao
authors.affiliation: Department of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL, USA.
authors.forename: Jared M
authors.initials: JM
authors.lastname: Osland
authors.affiliation: Department of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL, USA.|Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine, Springfield, IL, USA.
authors.forename: Xundi
authors.initials: X
authors.lastname: Chen
authors.affiliation: Department of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL, USA.|Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine, Springfield, IL, USA.
authors.forename: Skyler D
authors.initials: SD
authors.lastname: Gerber
authors.affiliation: Jiangsu 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.
authors.forename: Min
authors.initials: M
authors.lastname: Chen
authors.affiliation: Jiangsu 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.
authors.forename: Heng
authors.initials: H
authors.lastname: Gu
authors.affiliation: Department of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL, USA.
authors.forename: Rong
authors.initials: R
authors.lastname: Yuan
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics / Q000378:metabolism*; D000328:Adult; D000818:Animals; D016022:Case-Control Studies; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D008875:Middle Aged; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism*; D000078723:Nuclear Receptor Interacting Protein 1; D011565:Psoriasis / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D014162:Transfection; D055815:Young Adult
chemical_list: D048868:Adaptor Proteins, Signal Transducing; C000627127:NRIP1 protein, human; C000627128:Nrip1 protein, mouse; D009687:Nuclear Proteins; D000078723:Nuclear Receptor Interacting Protein 1
keywords: NRIP1; T cells; animal model; psoriasis; skin