Insightful exploring
            <scp>of microRNAs</scp>
            in psoriasis and its targeted topical delivery

Pradyuth, Sai K.; Rapalli, Vamshi Krishna; Gorantla, Srividya; Waghule, Tejashree; Dubey, Sunil Kumar; Singhvi, Gautam

doi:10.1111/dth.14221

Cited by 10 publications

(6 citation statements)

References 49 publications

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“…MicroRNAs (miRNAs/miRs) are a class of small, endogenous, single-stranded, non-coding RNAs that serve a key role in proliferation, apoptosis, differentiation, invasion and metabolism ( 7 ). miRNAs bind to the 3' untranslated regions (UTR) of specific target mRNAs via complementary base pairing, leading to mRNA degradation and the inhibition of translation ( 8 ).…”

Section: Introductionmentioning

confidence: 99%

miR‑489‑3p inhibits TLR4/NF‑κB signaling to prevent inflammation in psoriasis

Wang

Zhou

2021

Exp Ther Med

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Psoriasis is a chronic inflammatory skin disease whose etiology has not yet been determined. MicroRNAs (miRs) regulate the early stages of psoriasis and are targets for therapeutic intervention. The present study aimed to investigate the functional role of miR-489-3p in psoriasis. The present study first assessed the expression levels of miR-489-3p and Toll-like receptor (TLR)4 mRNA using reverse transcription-quantitative PCR, and also detected the protein expression levels of TLR4 and NF-κB via western blot analysis. TargetScan and miRDB target gene prediction tools were used to confirm the regulation of Toll-like receptor (TLR)4 by miR-489-3p. Moreover, a Cell Counting Kit (CCK)-8 assay was conducted to evaluate cell viability, while cell cycle and colony formation assays were performed to evaluate cell proliferation. Human keratinocytes (HaCaT) were co-transfected with TLR4-small interfering RNA and miR-489-3p-inhibitor plasmids, and analysis of cell proliferation and inflammatory cytokine secretion was performed using CCK-8 assay and ELISA. It was found that miR-489-3p expression was downregulated in patients with psoriasis. Bioinformatics analysis identified that TLR4 was a direct target of miR-489-3p. This was confirmed via luciferase reporter assays in HaCaT cells. The overexpression of miR-489-3p inhibited the TLR4/NF-κB signaling pathway and reduced cell proliferation. TLR4 silencing alleviated the effects of miR-489-3p, and enhanced cell proliferation and inflammatory cytokine secretion. Taken together, these data suggested that miR-489-3p may be a key effector of psoriasis, which promotes inflammatory responses by direct targeting of TLR4. miR-489-3p therefore represents a promising prognostic biomarker and therapeutic target for psoriasis treatment.

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Section: Introductionmentioning

confidence: 99%

miR‑489‑3p inhibits TLR4/NF‑κB signaling to prevent inflammation in psoriasis

Wang

Zhou

2021

Exp Ther Med

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“…Therefore, targeting specific miRNAs represents a potentially powerful tool which may prove to be useful in the development of novel therapeutic methods for psoriasis. 21,22 For example, miR-210 upregulation promoted psoriasis-like inflammation by augmenting Th1 and Th17 cell differentiation. 23 In addition, miR-146a could suppress skin inflammation in psoriasis.…”

Section: Discussionmentioning

confidence: 99%

EZH2 is involved in psoriasis progression by impairing miR-125a-5p inhibition of SFMBT1 and leading to inhibition of the TGFβ/SMAD pathway

Liu

Wang

2021

Therapeutic Advances in Chronic Disease

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Aims: In this study, we aimed to decipher the impact of enhancer of zeste homolog 2 (EZH2) in psoriasis as well as the underlying mechanism. Methods: A mouse model of psoriasis was developed by means of imiquimod induction, with the expression of EZH2, microRNA-125a-5p (miR-125a-5p), and SFMBT1 determined. The role of EZH2, miR-125a-5p, and SFMBT1 in malignant phenotypes of HaCaT cells and the development of psoriasis in vivo was subsequently investigated through gain- and loss-of-function experiments. Chromatin immunoprecipitation assay and dual-luciferase reporter assay were conducted to explore the relationship between EZH2 or SFMBT1 and miR-125a-5p. Finally, the effects of EZH2 and miR-125a-5p on the transforming growth factor β (TGFβ)/SMAD pathway were analyzed. Results: Overexpressed SFMBT1 and EZH2 was detected while miR-125a-5p were downregulated in psoriasis tissues and human keratinocyte (HaCaT) cells. EZH2 increased the levels of IL-17A-induced cytokines and promoted the malignant phenotypes of HaCaT cells. Functionally, EZH2 reduced miR-125a-5p expression while miR-125a-5p targeted SFMBT1 to activate the TGFβ/SMAD pathway in vitro. Knockdown of EZH2 or up-regulation of miR-125a-5p inhibited cell proliferation and the levels of IL-17A-induced cytokines, but increased the expression of TGFβ1 and the extent of smad2 and smad3 phosphorylation in HaCaT cells. Notably, EZH2 contributed to the development of psoriasis in vivo by inhibiting the TGFβ/SMAD pathway via impairment of miR-125a-5p-mediated SFMBT1 inhibition. Conclusion: Taken together, the results of the current study highlight the ability of EZH2 to potentially inactivate the TGFβ/SMAD pathway via upregulation of miR-125a-5p-dependent SFMBT1during the progression of psoriatic lesions.

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“…It has been reported potential role of microRNA (miRNA) in the management of psoriasis opened the way for miRNA-based targeted pharmacotherapy in psoriasis. Pradyuth et al suggested that the miRNA expression could be minimized as a potential biomarker to suppress the hyper-proliferation of keratinocytes and the production of inflammatory cytokine in the management of psoriasis [ 217 ]. The schematic illustration in Figure 8 highlights the delivery of miRNA through micelles/liposomes carrier system following the paracellular/transcellular route of absorption in skin and down-regulated epidermal homeostasis to achieve the goal of targeted pharmacotherapy through the inhibition of keratinocyte proliferation and inhibition of pro-inflammatory cytokine secretion.…”

Section: Targeted Pharmacotherapy In the Management Of Psoriasismentioning

confidence: 99%

“… Schematic illustration shows liposomes and micelles mediated targeted topical pharmacotherapy employing miRNA to decrease the pathological conditions over the skin in psoriasis. Reproduced from Pradyuth Sai et al [ 217 ], John Wiley and Sons, 2020. …”

Section: Figurementioning

confidence: 99%

Nanoscale Topical Pharmacotherapy in Management of Psoriasis: Contemporary Research and Scope

Ahmad

Mohammed

Algahtani

et al. 2022

JFB

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Psoriasis is a typical dermal condition that has been anticipated since prehistoric times when it was mistakenly implicit in being a variant of leprosy. It is an atypical organ-specific autoimmune disorder, which is triggered by the activation of T-cells and/or B-cells. Until now, the pathophysiology of this disease is not completely explicated and still, many research investigations are ongoing. Different approaches have been investigated to treat this dreadful skin disease using various anti-psoriatic drugs of different modes of action through smart drug-delivery systems. Nevertheless, there is no ideal therapy for a complete cure of psoriasis owing to the dearth of an ideal drug-delivery system for anti-psoriatic drugs. The conventional pharmacotherapy approaches for the treatment of psoriasis demand various classes of anti-psoriatic drugs with optimum benefit/risk ratio and insignificant untoward effects. The advancement in nanoscale drug delivery had a great impact on the establishment of a nanomedicine-based therapy for better management of psoriasis in recent times. Nanodrug carriers are exploited to design and develop nanomedicine-based therapy for psoriasis. It has a promising future in the improvement of the therapeutic efficacy of conventional anti-psoriatic drugs. The present manuscript aims to discuss the pathophysiology, conventional pharmacotherapy, and contemporary research in the area of nanoscale topical drug delivery systems for better management of psoriasis including the significance of targeted pharmacotherapy in psoriasis.

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Insightful exploring of microRNAs in psoriasis and its targeted topical delivery

Cited by 10 publications

References 49 publications

miR‑489‑3p inhibits TLR4/NF‑κB signaling to prevent inflammation in psoriasis

miR‑489‑3p inhibits TLR4/NF‑κB signaling to prevent inflammation in psoriasis

EZH2 is involved in psoriasis progression by impairing miR-125a-5p inhibition of SFMBT1 and leading to inhibition of the TGFβ/SMAD pathway

Nanoscale Topical Pharmacotherapy in Management of Psoriasis: Contemporary Research and Scope

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