Research Papers:

Expression and potential role of cellular retinol binding protein I in psoriasis

Gaetana Costanza, Elena Doldo, Amedeo Ferlosio, Chiara Tarquini, Daniela Passeri, Raffaella Cascella, Mauro Bavetta, Alessandro Di Stefani, Claudio Bonifati, Sara Agostinelli, Federica Centofanti, Emiliano Giardina, Elena Campione, Luca Bianchi, Pietro Donati, Aldo Morrone and Augusto Orlandi _

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Oncotarget. 2018; 9:36736-36749. https://doi.org/10.18632/oncotarget.26314

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Gaetana Costanza1,4,*, Elena Doldo1,*, Amedeo Ferlosio1,*, Chiara Tarquini1, Daniela Passeri1, Raffaella Cascella2, Mauro Bavetta3, Alessandro Di Stefani3, Claudio Bonifati4, Sara Agostinelli1, Federica Centofanti1, Emiliano Giardina2, Elena Campione3, Luca Bianchi3, Pietro Donati4, Aldo Morrone4 and Augusto Orlandi1,5

1Anatomic Pathology Unit, Department of Biomedicine and Prevention, Tor Vergata University of Rome, Rome, Italy

2Genetics Laboratory, Department of Biomedicine and Prevention, Tor Vergata University of Rome, Rome, Italy

3Dermatology Unit, Tor Vergata University of Rome, Policlinic of Tor Vergata of Rome, Rome, Italy

4San Gallicano Dermatology Institute, Rome, Italy

5Catholic University “Our Lady of Good Counsel”, Tirana, Albania

*These authors have contributed equally to this work

Correspondence to:

Augusto Orlandi, email: [email protected]

Keywords: CRBPI; retinoids; imiquimod-induced psoriasis; keratinocyte proliferation

Received: July 15, 2018    Accepted: October 25, 2018    Published: December 04, 2018


Psoriasis is a diffuse chronic skin disorder characterized from accelerated epidermal turnover and inflammatory cell infiltrate. Retinoids influence keratinocyte proliferation and differentiation as well as inflammatory response. Cellular retinol binding protein (CRBPI) regulates intracellular vitamin A bioavailability and contributes to maintain skin homeostasis. The aim of present study was to investigate the expression of CRBPI and its role in the pathogenesis of skin psoriasis. Immunohistochemistry revealed more diffuse and increased CRBPI expression in all epidermal layers of human psoriatic lesions except in the stratum corneum. An imiquimod-induced psoriatic-like model documented the increase of skin lesional area and severity index score as well as of the severity of microscopic features as parakeratosis, papillomatosis and spongiosis in CRBPI-knockout compared to wild-type mice, associated to the increased keratinocyte CK17 and Ki-67 expression and the reduction of CK1, CRABPII and RXRα. Gene array of imiquimod-induced psoriatic skin documented the greater up-regulation of EGF/PDGF-related genes and down-regulation of EGR1 and pro-inflammatory IL-related genes in CRBPI-knockout compared to wild-type mice. Finally, CRBPI transfection in HaCaT cells increased AKT and NF-κB-related genes and proteins and down-regulated IL-2, IL-6 and IL-8 pro-inflammatory signalling. Although not recognized as a psoriatic susceptibility gene in our cohort of patients, the present data strongly supported the potential role of CRBPI to sustain keratinocyte proliferation and differentiation and to counteract pro-inflammatory genes expression in psoriatic lesions.

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