MicroRNAs in Skin and Wound Healing

Banerjee, Jaideep; Sen, Chandan K.

doi:10.1007/978-1-62703-083-0_26

Cited by 61 publications

(51 citation statements)

References 47 publications

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“…The clinical utility of miRNAs as disease biomarkers has been studied in skin malignancy and has gained the attention of cutaneous fibrosis researchers. MiRNAs regulating skin fibrotic processes, such as let-7a, miRNA-7, miRNA-196a, and miRNA-150, have been detected in decreased levels in the serum of patients with scleroderma and affirm the potential of miRNA as a marker of the disease [3,10,18,23,24,42,69]. One study also demonstrated that serum levels of miRNA-142-3p are significantly higher in scleroderma patients [39].…”

Section: Clinical Applications Of Mirnas In Skin Fibrosismentioning

confidence: 99%

“…In combating skin fibrosis, anti-fibrotic miRNAs may be upregulated with the use of miRNA mimics or viral vectors [3,25]. Mimics are synthetic short double-stranded oligonucleotides, consisting of a guide strand and a passenger strand [3,17].…”

Section: Clinical Applications Of Mirnas In Skin Fibrosismentioning

confidence: 99%

“…Mimics are synthetic short double-stranded oligonucleotides, consisting of a guide strand and a passenger strand [3,17]. The guide strand has the same nucleotide sequence as the mature miRNA and is incorporated into the RISC complex [3,17]. The passenger strand is equivalent to miRNA* and complementary to the mature sequence [3,17].…”

Section: Clinical Applications Of Mirnas In Skin Fibrosismentioning

confidence: 99%

“…MiRNAs achieve this by interacting with the 3’ untranslated region (UTR) of target mRNAs (Figure 2) [53,56]. The interaction between the miRNA and mRNA results in one of two posttranscriptional mechanisms of gene regulation: mRNA degradation or translational repression [3,53,56]. The posttranscriptional mechanism utilized is dependent on the level of complementarity between the miRNA and the mRNA; significant complementarity results in mRNA degradation, while more limited complementarity favors translational repression [3].…”

Section: Introductionmentioning

confidence: 99%

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The role of microRNAs in skin fibrosis

et al. 2013

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Fibrotic skin disorders may be debilitating and impair quality of life. There are few effective treatment options for cutaneous fibrotic diseases. In this review, we discuss our current understanding of the role of microRNAs (miRNAs) in skin fibrosis. MiRNAs are a class of small, noncoding RNAs involved in skin fibrosis. These small RNAs range from 18 to 25 nucleotides in length and modify gene expression by binding to target messenger RNA (mRNA), causing degradation of the target mRNA or inhibiting the translation into proteins. We present an overview of the biogenesis, maturation and function of miRNAs. We highlight miRNA’s role in key skin fibrotic processes including: transforming growth factor (TGF)-beta signaling, extracellular matrix (ECM) deposition, and fibroblast proliferation and differentiation. Some miRNAs are profibrotic and their upregulation favors these processes contributing to fibrosis, while antifibrotic miRNAs inhibit these processes and may be reduced in fibrosis. Finally we describe the diagnostic and therapeutic significance of miRNAs in the management of skin fibrosis. The discovery that miRNAs are detectable in serum, plasma, and other bodily fluids, and are relatively stable, suggests miRNAs may serve as valuable biomarkers to monitor disease progression and response to treatment. In the treatment of skin fibrosis, antifibrotic miRNAs may be upregulated using mimics and viral vectors. Conversely, profibrotic miRNAs may be downregulated by employing anti-miRNAs, sponges, erasers and masks. We believe that miRNA-based therapies hold promise as important treatments and may transform the management of fibrotic skin diseases by physicians.

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Section: Clinical Applications Of Mirnas In Skin Fibrosismentioning

confidence: 99%

Section: Clinical Applications Of Mirnas In Skin Fibrosismentioning

confidence: 99%

Section: Clinical Applications Of Mirnas In Skin Fibrosismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The role of microRNAs in skin fibrosis

et al. 2013

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“…It also regulates MMP-2 via the PTEN pathway as a result of myocardial infarction 44 . Inhibition of the PTEN pathway also activates many downstream targets, such as mTOR, which regulates protein synthesis, glucose homeostasis, autophagy, and proliferation (Figure 2).…”

Section: Main Textmentioning

confidence: 99%

MicroRNA as Therapeutic Targets for Chronic Wound Healing

Mulholland

Dunne

McCarthy

2017

Molecular Therapy - Nucleic Acids

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Wound healing is a highly complex biological process composed of three overlapping phases: inflammation, proliferation, and remodeling. Impairments at any one or more of these stages can lead to compromised healing. MicroRNAs (miRs) are non-coding RNAs that act as post-transcriptional regulators of multiple proteins and associated pathways. Thus, identification of the appropriate miR involved in the different phases of wound healing could reveal an effective third-generation genetic therapy in chronic wound care. Several miRs have been shown to be upregulated or downregulated during the wound healing process. This article examines the biological processes involved in wound healing, the miR involved at each stage, and how expression levels are modulated in the chronic wound environment. Key miRs are highlighted as possible therapeutic targets, either through underexpression or overexpression, and the healing benefits are interrogated. These are prime miR candidates that could be considered as a gene therapy option for patients suffering from chronic wounds. The success of miR as a gene therapy, however, is reliant on the development of an appropriate delivery system that must be designed to overcome both extracellular and intracellular barriers.

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miRNA‐126 enhances viability, colony formation, and migration of keratinocytes HaCaT cells by regulating PI3 K/AKT signaling pathway

Chang

Liang

Xia

et al. 2019

Cell Biology International

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Wound healing is a basic biological process including proliferation and migration of keratinocyte. The effects of microRNAs on skin wound healing remain largely unexplored. This study aimed to investigate the role of microRNA-126 (miR-126) in human skin wound healing. Relative expression of miR-126 after injury was evaluated by qRT-PCR. Cell viability, colony formation, cycle distribution, migration, and the alternation of PI3 K/AKT pathway after miR-126 knockdown or overexpression were detected, respectively. In addition, potential target gene of miR-126 was also explored by luciferase assay. Results showed that miR-126 was up-regulated during skin wound healing. Moreover, overexpression of miR-126 promoted cell proliferation and migration, whereas inhibition of miR-126 led to the opposite effects. Additionally, we discovered that PLK2, which inhibited cell viability, colony formation and migration of keratinocyte, was a target gene of miR-126. The expression of PLK2 was negatively correlated with the level of miR-126 during wound healing. Finally, we demonstrated that overexpression of miR-126 significantly increased the expression of p-AKT, p-ERK2, and PI3 K, indicating that overexpression of miR-126 activated PI3 K/AKT signaling pathway. In conclusion, our results demonstrated that miR-126 acted as a critical regulator for promoting proliferation and migration in keratinocyte during skin wound healing. contributed equally to this work. Abbreviations: 3 0 UTR, 3 0 -untranslated regions; CDK, cyclin-dependent kinases; EGFL7, epidermal growth factor-like domain 7; IRS-1, insulin receptor substrate-1; miR-126, microRNA-126; p-AKT, phosphorylated protein kinase B; p-ERK2, phosphorylated extracellular signal-regulated kinase 2

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MicroRNAs in Skin and Wound Healing

Cited by 61 publications

References 47 publications

The role of microRNAs in skin fibrosis

The role of microRNAs in skin fibrosis

MicroRNA as Therapeutic Targets for Chronic Wound Healing

miRNA‐126 enhances viability, colony formation, and migration of keratinocytes HaCaT cells by regulating PI3 K/AKT signaling pathway

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