LncRNA UCA1 negatively regulates NF‐kB activity in psoriatic keratinocytes through the miR125a‐A20 axis
Psoriasis is one of the most common chronic inflammatory skin diseases that affects approximately 3% of the world's population. Hyper proliferation, infiltration of inflammatory cells and aberrant differentiation of keratinocytes are the three most important characteristics of psoriasis. Previo...
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Published in | The Kaohsiung journal of medical sciences Vol. 37; no. 3; pp. 172 - 180 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
BP, Asia
Wiley Publishing Asia Pty Ltd
01.03.2021
John Wiley & Sons, Inc Wiley |
Subjects | |
Online Access | Get full text |
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Summary: | Psoriasis is one of the most common chronic inflammatory skin diseases that affects approximately 3% of the world's population. Hyper proliferation, infiltration of inflammatory cells and aberrant differentiation of keratinocytes are the three most important characteristics of psoriasis. Previous reports showed that NF‐κBis the crucial mediator linking psoriatic keratinocytes and immune cell states through its effects on chemokine and cytokine production. To identify the role of NF‐κB in psoriasis, we conducted ELISA assay to detect the activity of NF‐κB in lesional skin and nonlesional skin of patients with psoriasis. Mounting evidence suggests that the interaction between long noncoding RNAs (lncRNAs) and microRNAs plays important role in the regulation of the initiation and development of various diseases. In this article, we identified that lncRNA UCA1 was down‐regulated in lesional skin of patients with psoriasis. Further studies showed that lncRNA UCA1 could promote the expression of A20 by inhibitingmiR125a, and up‐regulated A20 decreased the activity of NF‐κB through its ubiquitin editing function. Taken together, we identified and demonstrated that lncRNA UCA1 negatively regulated NF‐κB activity in psoriasis through the miR125a‐A20 axis. |
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Bibliography: | Funding information Grant from Peking University International Hospital, Grant/Award Number: YN2018QN04; National Natural Science Foundation of China, Grant/Award Number: 81773311 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1607-551X 2410-8650 |
DOI: | 10.1002/kjm2.12363 |