MiR‐126 correlates with increased disease severity and promotes keratinocytes proliferation and inflammation while suppresses cells' apoptosis in psoriasis

Feng, Shike; Wang, Lin; Liu, Wang; Zhong, Yan; Xu, Shen

doi:10.1002/jcla.22588

Cited by 22 publications

(18 citation statements)

References 26 publications

(58 reference statements)

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“… 6 , 7 In recent years, physiotherapy, topical therapy, and systemic therapy are the main therapeutic strategies for the treatment of psoriasis. 8 However, the treatment options for treating patients with psoriasis remain unsatisfactory due to the low response rate and high recurrence rate. 8 Therefore, it is important to explore better therapeutic strategies for the treatment of psoriasis.…”

Section: Introductionmentioning

confidence: 99%

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<p>Triptolide Inhibits the Proliferation of HaCaT Cells Induced by IL22 via Upregulating miR-181b-5p</p>

He¹,

Zhang²,

Hu³

et al. 2020

DDDT

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Background Evidence has been shown that triptolide was effective in the treatment of psoriasis; however, the mechanisms remain poorly understood. Thus, this study aimed to investigate the role of triptolide on the proliferation and differentiation of HaCaT cells which are treated with IL22 to mimic abnormal proliferation/differentiation in keratinocyte of psoriasis. Materials and Methods HaCaT cells were transfected with miR-181b-5p antagomir for 24 h, and then exposed to 10 μM Triptolide for 24 h, following by 100 ng/mL of IL22 for 24 h. In addition, the proliferation and cell cycle distribution in HaCaT cells were assessed by immunofluorescence or flow cytometry assays, respectively. Results Triptolide obviously upregulated the level of miR-181b-5p in HaCaT cells. In addition, triptolide significantly inhibited IL22-induced proliferation of HaCaT cells via inducing cell cycle arrest. Moreover, IL22 markedly inhibited the differentiation of HaCaT cells, and this phenomenon was reversed by triptolide treatment. In contrast, the effects of triptolide on the proliferation and differentiation in IL22-stimulated HaCaT cells were notably reversed by miR-181b-5p antagomir. Moreover, dual-luciferase assay showed that E2F5 was the direct target of miR-181b-5p in HaCaT cells. Meanwhile, upregulation of miR-181b-5p obviously decreased the level of E2F5 in HaCaT cells. Conclusion In this study, we found that triptolide could inhibit the proliferation and promote the differentiation in IL22-stimulated keratinocytes via upregulating miR-181b-5p. These data indicated that triptolide may be a potential agent for the treatment of psoriasis.

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Section: Introductionmentioning

confidence: 99%

“… 8 However, the treatment options for treating patients with psoriasis remain unsatisfactory due to the low response rate and high recurrence rate. 8 Therefore, it is important to explore better therapeutic strategies for the treatment of psoriasis.…”

Section: Introductionmentioning

confidence: 99%

<p>Triptolide Inhibits the Proliferation of HaCaT Cells Induced by IL22 via Upregulating miR-181b-5p</p>

He¹,

Zhang²,

Hu³

et al. 2020

DDDT

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“…Forced over-expression of miR-126 has increased cell proliferation and reduced apoptosis in HaCaT cells. These effects were accompanied by over-production of TNF-α, IFN-γ, IL-17A, and IL-22 while down-regulation of IL-10 levels [ 42 ]. In addition, expression levels of miR-146a and miR-146b have been increased in the psoriatic lesions.…”

Section: Up-regulated Mirnas In Psoriasismentioning

confidence: 99%

“… Keratinocytes C‐caspase, Bcl‐2, TNF‐α, IFN‐γ, IL‐17A and IL‐22 Apoptosis Upregulation of miR‐126 promotes cells proliferation and inflammation while prevents cells apoptosis in keratinocytes. [ 42 ] miR-146a/b 30 patients with psoriasis and 30 control subjects were included in the study. Human epidermal keratinocytes (HEKs) FERMT1, IRAK1, CCL5, IL-8, CARD10 and NUMB NF-κB signaling pathway and regulation of cell proliferation The ability of miR-146a/b to hinder inflammatory responses, activation-induced cell death and proliferation of keratinocytes and fibroblasts proposes that miR-146a/b participate in the skin homeostasis and controlling inflammatory responses in both healthy and diseased skin.…”

Section: Up-regulated Mirnas In Psoriasismentioning

confidence: 99%

The eminent roles of ncRNAs in the pathogenesis of psoriasis

Ghafouri‐Fard

Eghtedarian

Taheri

et al. 2020

Non-coding RNA Research

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Psoriasis is a chronic immune-related disorder in which both genetic and environmental parameters are involved. Recent studies have demonstrated dysregulation of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) in the peripheral blood or skin lesions of patients with psoriasis. While a number of lncRNAs such as MEG3, AL162231.4 and NONHSAT044111 have been down-regulated in the course of psoriasis, others including PRINS, MIR31HG, RP6‐65G23.1, MSX2P1, SLC6A14-1:1, NR_003062 have been up-regulated. Moreover, expressions of several miRNAs have been dysregulated in this disorder. Among dysregulated miRNAs are miR-126, miR-143, miR-19a and miR-155 whose diagnostic roles in the psoriasis have also been assessed. Dysregulated non-coding RNAs in this disorder participate in the regulation of chemokine signaling pathway and immune response, control of epidermal development and skin barrier as well as modulation of function of certain subsets of T cells. Besides, these transcripts possibly regulate activity of NF-κΒ, mTOR, MAPK and JAK-STAT signaling pathways. Besides, expression levels of circRNAs have been decreased in the psoriasis lesions. Massive alterations in the levels of lncRNAs and miRNAs in the psoriasis lesions or peripheral blood of affected individuals show participation of these transcripts in the pathogenesis of this disorder.

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“…MiR-126 is located in intron 7 of egfl7 and plays important roles in angiogenesis and inflammation [28][29][30]. In most human cancers, miR-126 functions as a tumour suppressor, and studies have revealed the downregulation of miR-126 in cancerous tissues compared with noncancerous tissues [31][32][33][34].…”

Section: Discussionmentioning

confidence: 99%

Polymorphisms in miRNA genes play roles in the initiation and development of cervical cancer

Zhang¹,

Zhou²,

Li³

et al. 2019

J. Cancer

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MicroRNA deregulation is crucial for cancer development. Studies showed that polymorphisms in miRNA genes could affect miRNA expression, which might be associated with cancer development. In the current study, we investigated the association of seven single nucleotide polymorphisms (SNPs) in seven miRNA genes with the initiation and development of cervical cancer in a Chinese Han population. The SNPs of 358 cervical intraepithelial neoplasia (CIN) patients, 547 cervical cancer patients and 567 healthy individuals were genotyped using TaqMan assays. Moreover, we evaluated the association of the seven SNPs with the different stages of cervical cancer. Our results showed that rs4636297 in miR-126 was associated with susceptibility to CIN and cervical cancer (P=0.019 and 0.019, respectively) and that the T allele was associated with a higher risk of CIN (OR=1.334, 95% CI: 1.049-1.698) and cervical cancer (OR=1.296, 95% CI: 1.044-1.609). Similarly, rs11614913 in miR-125a was associated with CIN and cervical cancer (P=0.025 and 0.015, respectively), and the T allele might be the protective factor for CIN (OR=0.807, 95% CI: 0.669-0.974) and cervical cancer (OR=0.814, 95% CI: 0.689-0.961). Our results indicated that rs4636297 in miR-126 and rs11614913 in miR-196a2 play an important role only in the initiation of cervical cancer not in the development of CIN to cervical cancer.

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MiR‐126 correlates with increased disease severity and promotes keratinocytes proliferation and inflammation while suppresses cells' apoptosis in psoriasis

Abstract: In conclusion, miR-126 correlates with elevated risk and increased disease severity in psoriasis patients, and upregulation of miR-126 promotes cells' proliferation and inflammation while inhibits cells' apoptosis in keratinocytes.

Cited by 22 publications

References 26 publications

<p>Triptolide Inhibits the Proliferation of HaCaT Cells Induced by IL22 via Upregulating miR-181b-5p</p>

<p>Triptolide Inhibits the Proliferation of HaCaT Cells Induced by IL22 via Upregulating miR-181b-5p</p>

The eminent roles of ncRNAs in the pathogenesis of psoriasis

Polymorphisms in miRNA genes play roles in the initiation and development of cervical cancer

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