miR-23b promotes cutaneous wound healing through inhibition of the inflammatory responses by targeting ASK1

Zhang, Lipeng; Han, Xiao; Zuo, Kuiyang; Li, Li; Liu, Jieting; Yuan, Xin; Shen, Yongchao; Shao, Ming; Pang, Daxin; Chu, Yanhui; Zhao, Binghai

doi:10.1093/abbs/gmy109

Cited by 22 publications

(15 citation statements)

References 40 publications

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“…Sar1A, Smad2, TNF-α 2 , and IL-8 3 [137] hsa-miR-149-5p Downregulates keratinocyte inflammatory cytokine expression IL-1α, IL-1β, and IL-6 [138] hsa-miR-17-5p Downregulates keratinocyte inflammatory cytokine expression Not shown [139] hsa-miR-23b-3p Inhibits keratinocyte-derived pro-inflammatory cytokines ASK1 4 [140] hsa-miR-31-5p Promotes keratinocyte proliferation and migration EMP-1 5 [141] mmu-miR-31-5p Promotes keratinocyte proliferation and migration Rasa1 6 , Spred1 7 , Spred2, and Spry4 8 [142] dre-mir-223…”

Section: Functions Major Targets Referencesmentioning

confidence: 99%

“…The stimulation of keratinocytes by LPS triggers an inflammatory response and the expression of miR-17 while silencing miR-17 decreases cell viability and stimulates keratinocyte cytokine expression [139]. The levels of miR-31, miR-23b, and miR-223 are increased in keratinocytes after wounding [140,142,143]. MiR-223 suppresses NF-κB activation specifically in basal epithelial cells and dampens excessive neutrophil recruitment to the site of injury in a zebrafish wound model [143].…”

Section: Functions Major Targets Referencesmentioning

confidence: 99%

“…MiR-31 promotes keratinocyte proliferation and migration by activating MAPK signaling, and epidermis-specific depletion of miR-31 delays wound healing in vivo [142]. In addition, miR-23b promotes wound healing by increasing keratinocyte proliferation and suppressing cytokine production [140]. The miRNAs that regulate keratinocyte immune functions and play a pathological role in chronic wounds are summarized in Section 5.4.…”

Section: Functions Major Targets Referencesmentioning

confidence: 99%

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The Immune Functions of Keratinocytes in Skin Wound Healing

Piipponen

Landén

2020

IJMS

251

139

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As the most dominant cell type in the skin, keratinocytes play critical roles in wound repair not only as structural cells but also exerting important immune functions. This review focuses on the communications between keratinocytes and immune cells in wound healing, which are mediated by various cytokines, chemokines, and extracellular vesicles. Keratinocytes can also directly interact with T cells via antigen presentation. Moreover, keratinocytes produce antimicrobial peptides that can directly kill the invading pathogens and contribute to wound repair in many aspects. We also reviewed the epigenetic mechanisms known to regulate keratinocyte immune functions, including histone modifications, non-protein-coding RNAs (e.g., microRNAs, and long noncoding RNAs), and chromatin dynamics. Lastly, we summarized the current evidence on the dysregulated immune functions of keratinocytes in chronic nonhealing wounds. Based on their crucial immune functions in skin wound healing, we propose that keratinocytes significantly contribute to the pathogenesis of chronic wound inflammation. We hope this review will trigger an interest in investigating the immune roles of keratinocytes in chronic wound pathology, which may open up new avenues for developing innovative wound treatments.

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Section: Functions Major Targets Referencesmentioning

confidence: 99%

Section: Functions Major Targets Referencesmentioning

confidence: 99%

Section: Functions Major Targets Referencesmentioning

confidence: 99%

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The Immune Functions of Keratinocytes in Skin Wound Healing

Piipponen

Landén

2020

IJMS

251

139

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“…Previous studies have shown that significant changes in miRNA expression, such as miR-23b [14], miR-146a [15], miR-150 [16], and miR-223 [17], are associated with sepsis. miR-23b, a multifunctional miRNA, has emerged as an anti-inflammatory factor that contributes to the modulation of multiple signaling pathways, in which the molecules regulate dozens of proinflammatory cytokines [18, 19]. Zhu et al showed a significant decrease in miR-23b expression in patients with rheumatoid arthritis as well as in animal models of multiple sclerosis and rheumatoid arthritis, and miR-23b prevented various inflammatory autoimmune diseases by targeting IL-17 [20].…”

Section: Introductionmentioning

confidence: 99%

miR-23b Negatively Regulates Sepsis-Induced Inflammatory Responses by Targeting ADAM10 in Human THP-1 Monocytes

Zhang

Xie

et al. 2019

Mediators of Inflammation

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Background Previous studies have demonstrated pivotal roles of disintegrin and metalloproteinase 10 (ADAM10) in the pathogenesis of sepsis. MicroRNA- (miR-) 23b has emerged as an anti-inflammatory factor that prevents multiple autoimmune diseases. However, the underlying mechanisms of miR-23b in the regulation of ADAM10 and sepsis remain uncharacterized. Methods The expression levels of ADAM10 and miR-23b were detected by quantitative RT-PCR and western blot analysis. Cytokine production and THP-1 cell apoptosis were measured by enzyme-linked immunosorbent and annexin V apoptosis assays. Bioinformatics analyses and qRT-PCR, western blot, and luciferase reporter assays were performed to identify ADAM10 as the target gene of miR-23b. Results miR-23b expression was downregulated in the peripheral blood mononuclear cells of sepsis patients and LPS-induced THP-1 cells and was negatively correlated with the expression of ADAM10 and inflammatory cytokines. miR-23b regulated ADAM10 expression by directly binding to the 3′-UTR of ADAM10 mRNA. The overexpression of miR-23b alleviated the LPS-stimulated production of inflammatory cytokines (TNF-α, IL-1β, and IL-6) and apoptosis by targeting ADAM10 in THP-1 cells. The inhibitor or knockdown of ADAM10 elicited effects similar to those of miR-23b on THP-1 cells upon LPS stimulation. Conclusions The present study demonstrated that miR-23b negatively regulated LPS-induced inflammatory responses by targeting ADAM10. The molecular regulatory mechanism of miR-23b in ADAM10 expression and sepsis-induced inflammatory consequences may provide potential therapeutic targets for sepsis.

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“…miR-23b, which is a differentiation marker of human keratinocytes (through repression of TGIF1 and activation of the TGF-β-SMAD2 signaling pathway), is remarkably upregulated after UVA irradiation of human primary keratinocytes and acts through targeting-related RAS viral oncogene homolog 2 (RRAS2), which is strongly expressed in highly aggressive malignant skin cancer [39,40]. Moreover, miR-23b promotes cutaneous wound healing through inhibition of the inflammatory responses by targeting ASK1 [41].…”

mentioning

confidence: 99%

MicroRNA Expression in Cutaneous Lupus: A New Window to Understand Its Pathogenesis

Méndez‐Flores

Furuzawa‐Carballeda

Hernández-Molina

et al. 2019

Mediators of Inflammation

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Background. The role of miRNAs in the pathogenesis of cutaneous lupus has not been studied. Objective. It was to assess the levels of a selected panel of circulating miRNAs that could be involved in the regulation of the immune response, inflammation, and fibrosis in cutaneous lupus. Methods. It was a cross-sectional study. We included 22 patients with subacute (SCLE) and 20 with discoid (DLE) lesions, and 19 healthy donors (HD). qRT-PCR for miRNA analysis, flow cytometry in peripheral blood, and skin immunohistochemistry were performed to determine the distribution of CD4 T cells and regulatory cells and their correlation with circulating miRNAs. Results. miR-150, miR-1246, miR-21, miR-23b, and miR-146 levels were downregulated in SCLE vs. HD. miR-150, miR-1246, and miR-21 levels were downregulated in DLE vs. HD. Peripheral CD4+/CD25-/IL-4+ cells and CD4+/CD25hi/Foxp3+ were negatively associated with miR-23b, and CD4+/CD25-/IFN-γ+ with miR-1246 in SCLE, whereas CD123+/CD196+/IDO+ cells were positively associated with miR-150 in DLE. In the tissue, CD4+/IL-4+ and CD20+/IL-10+ cells were positively associated with miR-21 and CD4+/IFN-γ+ with miR-31 in SCLE, whereas CD4+/IL-4+ cells were positively associated with miR-150, and CD20+/IL-10+ cells with miR-1246 and miR-146a in DLE. In the SCLE, lower miR-150 levels were correlated with higher CLASI scores. The KEGG pathway enrichment analysis revealed that cell cycle regulation pathways, p53, TGF-β, thyroid hormone, and cancer signaling pathways were shared between miR-21, miR-31, miR-23b, miR-146a, miR-1246, and miR-150. Conclusions. A downregulation of miR-150, miR-1246, and miR-21 in both CLE varieties vs. HD was determined.

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miR-23b promotes cutaneous wound healing through inhibition of the inflammatory responses by targeting ASK1

Cited by 22 publications

References 40 publications

The Immune Functions of Keratinocytes in Skin Wound Healing

The Immune Functions of Keratinocytes in Skin Wound Healing

miR-23b Negatively Regulates Sepsis-Induced Inflammatory Responses by Targeting ADAM10 in Human THP-1 Monocytes

MicroRNA Expression in Cutaneous Lupus: A New Window to Understand Its Pathogenesis

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