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MicroRNA-31 is over...
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Xu, NingKarolinska Institutet
(författare)
MicroRNA-31 is overexpressed in psoriasis and modulates inflammatory cytokine and chemokine production in keratinocytes via targeting serine/threonine kinase 40.
- Artikel/kapitelEngelska2013
Förlag, utgivningsår, omfång ...
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2013-01-15
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The American Association of Immunologists,2013
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printrdacarrier
Nummerbeteckningar
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LIBRIS-ID:oai:DiVA.org:uu-421680
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-421680URI
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https://doi.org/10.4049/jimmunol.1202695DOI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:125953649URI
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Språk:engelska
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Sammanfattning på:engelska &language:-1_t
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Klassifikation
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Ämneskategori:ref swepub-contenttype
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Ämneskategori:art swepub-publicationtype
Anmärkningar
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Psoriasis is characterized by a specific microRNA expression profile, distinct from that of healthy skin. MiR-31 is one of the most highly overexpressed microRNAs in psoriasis skin; however, its biological role in the disease has not been studied. In this study, we show that miR-31 is markedly overexpressed in psoriasis keratinocytes. Specific inhibition of miR-31 suppressed NF-κB-driven promoter luciferase activity and the basal and TNF-α-induced production of IL-1β, CXCL1/growth-related oncogene-α, CXCL5/epithelial-derived neutrophil-activating peptide 78, and CXCL8/IL-8 in human primary keratinocytes. Moreover, interference with endogenous miR-31 decreased the ability of keratinocytes to activate endothelial cells and attract leukocytes. By microarray expression profiling, we identified genes regulated by miR-31 in keratinocytes. Among these genes, we identified serine/threonine kinase 40 (STK40), a negative regulator of NF-κB signaling, as a direct target for miR-31. Silencing of STK40 rescued the suppressive effect of miR-31 inhibition on cytokine/chemokine expression, indicating that miR-31 regulates cytokine/chemokine expression via targeting STK40 in keratinocytes. Finally, we demonstrated that TGF-β1, a cytokine highly expressed in psoriasis epidermis, upregulated miR-31 expression in keratinocytes in vitro and in vivo. Collectively, our findings suggest that overexpression of miR-31 contributes to skin inflammation in psoriasis lesions by regulating the production of inflammatory mediators and leukocyte chemotaxis to the skin. Our data indicate that inhibition of miR-31 may be a potential therapeutic option in psoriasis.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
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Meisgen, FlorianKarolinska Institutet
(författare)
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Butler, Lynn MKarolinska Institutet
(författare)
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Han, Gangwen
(författare)
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Wang, Xiao-Jing
(författare)
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Söderberg-Nauclér, CeciliaKarolinska Institutet
(författare)
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Ståhle, MonaKarolinska Institutet
(författare)
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Pivarcsi, AndorKarolinska Institutet(Swepub:uu)andpi932
(författare)
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Sonkoly, EniköKarolinska Institutet(Swepub:uu)enipi547
(författare)
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Karolinska Institutet
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Journal of Immunology: The American Association of Immunologists190:2, s. 678-880022-17671550-6606
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