MicroRNA-378a-3p is overexpressed in psoriasis and modulates cell cycle arrest in keratinocytes via targeting BMP2 gene

Wipasiri Soonthornchai; Pattarin Tangtanatakul; Kornvalee Meesilpavikkai; Virgil Dalm; Patipark Kueanjinda; Jongkonnee Wongpiyabovorn

doi:10.1038/s41598-021-93616-8

MicroRNA-378a-3p is overexpressed in psoriasis and modulates cell cycle arrest in keratinocytes via targeting BMP2 gene

Wipasiri Soonthornchai, Pattarin Tangtanatakul, Kornvalee Meesilpavikkai, Virgil Dalm, Patipark Kueanjinda, Jongkonnee Wongpiyabovorn^*

^*Corresponding author for this work

Internal Medicine

Research output: Contribution to journal › Article › Academic › peer-review

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Abstract

Psoriasis is a chronic autoimmune skin disease driven by dysregulations at the cellular, genomic and genetic levels. MicroRNAs are key mediators of gene expression regulation. However, how microRNAs control the pathogenesis of psoriasis is still unclear. Here, we reported a significant up-regulation of miR-378a-3p (miR-378a) in skin biopsies from active psoriatic lesions while it was down-regulated after treatment with methotrexate or narrow-band ultraviolet B phototherapy. Using the keratinocyte in vitro model, we showed that miR-378a disturbed the cell cycle progression, causing cell cycle arrest at G1 phase. Transcriptomic analysis of keratinocytes with miR-378a overexpression and depletion revealed several important biological mechanisms related to inflammation and tight junction. Target mRNA transcript assessed by luciferase assay identified bone morphogenetic protein 2 as a novel target gene of miR-378a. These findings offer a mechanistic model where miR-378a contributes to the pathogenesis of psoriasis.

Original language	English
Article number	14186
Journal	Scientific Reports
Volume	11
Issue number	1
DOIs	https://doi.org/10.1038/s41598-021-93616-8
Publication status	Published - 9 Jul 2021

Bibliographical note

Funding Information:
This work was supported by a research grant from the Government Research Budget (2016), Thailand Research Fund (TRG 5480010), and the Ratchadapisaek Sompote Post-Doctoral Fund, Chulalongkorn University.

Publisher Copyright:
© 2021, The Author(s).

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MicroRNA-378a-3p is overexpressed in psoriasis and modulates cell cycle arrest in keratinocytes via targeting BMP2 geneFinal published version, 4.08 MBLicence: CC BY

Cite this

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title = "MicroRNA-378a-3p is overexpressed in psoriasis and modulates cell cycle arrest in keratinocytes via targeting BMP2 gene",

abstract = "Psoriasis is a chronic autoimmune skin disease driven by dysregulations at the cellular, genomic and genetic levels. MicroRNAs are key mediators of gene expression regulation. However, how microRNAs control the pathogenesis of psoriasis is still unclear. Here, we reported a significant up-regulation of miR-378a-3p (miR-378a) in skin biopsies from active psoriatic lesions while it was down-regulated after treatment with methotrexate or narrow-band ultraviolet B phototherapy. Using the keratinocyte in vitro model, we showed that miR-378a disturbed the cell cycle progression, causing cell cycle arrest at G1 phase. Transcriptomic analysis of keratinocytes with miR-378a overexpression and depletion revealed several important biological mechanisms related to inflammation and tight junction. Target mRNA transcript assessed by luciferase assay identified bone morphogenetic protein 2 as a novel target gene of miR-378a. These findings offer a mechanistic model where miR-378a contributes to the pathogenesis of psoriasis.",

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AU - Soonthornchai, Wipasiri

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AU - Dalm, Virgil

AU - Kueanjinda, Patipark

AU - Wongpiyabovorn, Jongkonnee

N1 - Funding Information: This work was supported by a research grant from the Government Research Budget (2016), Thailand Research Fund (TRG 5480010), and the Ratchadapisaek Sompote Post-Doctoral Fund, Chulalongkorn University. Publisher Copyright: © 2021, The Author(s).

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MicroRNA-378a-3p is overexpressed in psoriasis and modulates cell cycle arrest in keratinocytes via targeting BMP2 gene

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