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MiR‐21 is up‐regulated in psoriasis and suppresses T cell apoptosis
Author(s) -
Meisgen Florian,
Xu Ning,
Wei Tianling,
Janson Peter C.,
Obad Susanna,
Broom Oliver,
Nagy Nikoletta,
Kauppinen Sakari,
Kemény Lajos,
Ståhle Mona,
Pivarcsi Andor,
Sonkoly Enikö
Publication year - 2012
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2012.01462.x
Subject(s) - psoriasis , microrna , apoptosis , inflammation , cancer research , biology , microbiology and biotechnology , immunology , gene , genetics
MicroRNAs are short non‐coding RNAs that regulate gene expression. Previously, in a genome‐wide screen, we found deregulation of microRNA expression in psoriasis skin. MicroRNA‐21 (miR‐21) is one of the microRNAs significantly up‐regulated in psoriasis skin lesions. To identify the cell type responsible for the increased miR‐21 level, we compared expression of miR‐21 in epidermal cells and dermal T cells between psoriasis and healthy skin and found elevated levels of miR‐21 in psoriasis in both cell types. In cultured T cells, expression of miR‐21 increased markedly upon activation. To explore the function of miR‐21 in primary human T helper cells, we inhibited miR‐21 using a tiny seed‐targeting LNA‐anti‐miR. Specific inhibition of miR‐21 increased the apoptosis rate of activated T cells. Our results suggest that miR‐21 suppresses apoptosis in activated T cells, and thus, overexpression of miR‐21 may contribute to T cell–derived psoriatic skin inflammation.