Ginsenoside (Rg-1) promoted the wound closure of diabetic foot ulcer through iNOS elevation via miR-23a/IRF-1 axis

Cai, Hongbin; Huang, Liang; Zheng, Lijun; Fu, Kun; Wang, Jing; Hu, Feng-Dan; Liao, Ruo-Yi

doi:10.1016/j.lfs.2019.05.081

Cited by 42 publications

(20 citation statements)

References 25 publications

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“…Human umbilical vein endothelial cells (HUVECs, Cell Bank of the Chinese Academy of Sciences, Shanghai, China) were cultured in F12 medium (Gibco BRL) containing 10% FBS (Gibco BRL). In order to mimic diabetic environment in vitro, high glucose cultured HUVECs (HG-HUVECs) had confirmed to be often employed and obtained by using high glucose (HG;40 mM) to treat HUVECs for 72 h (the media were changed every 24 h), as previously described [22,23]. To further explore Exos-induced anti-inflammation effects in the cells, lipopolysaccharide (LPS) was used as an activator of the inflammatory response to induce enhanced inflammation and combined with Exos to treat cells [24].…”

Section: Methodsmentioning

confidence: 99%

Macrophage-derived exosomes accelerate wound healing through their anti-inflammation effects in a diabetic rat model

Wang

Tian

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

141

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Chronic, subclinical inflammation was often observed in the diabetic wound area, causing inadequate and delayed wound-healing effects by failing to initiate cell migration, proliferation, and extracellular matrix deposition. Therefore, we presented macrophage-derived exosomes (Exos) and explored their potential for inhibiting inflammation and accelerating diabetic wound healing in a skin defect, diabetic rat model. A thorough investigation demonstrated that Exos exerted anti-inflammatory effects by inhibiting the secretion of pro-inflammatory enzymes and cytokines. Furthermore, they accelerated the wound-healing process by inducing endothelial cell proliferation and migration to improve angiogenesis and re-epithelialization in diabetic wounds. ARTICLE HISTORY

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Section: Methodsmentioning

confidence: 99%

Macrophage-derived exosomes accelerate wound healing through their anti-inflammation effects in a diabetic rat model

Wang

Tian

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

141

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“…The SP1 transcriptional regulatory element is present within the TLR4, TNF-α, and TGF-β1 gene promoters, while the IRF1 transcriptional regulatory element is present within the IL10 gene promoter [20][21][22][23]. Furthermore, SP1 and IRF1 have been shown to be direct targets of miR-23a in previous studies [24][25][26]. Thus, it is reasonable to infer that miR-23a-3p could mediate the imbalance between TLR4/TNF-α pro-inflammatory and IL10/TGF-β1 anti-inflammatory pathways under Mtb stimuli via targeting SP1 and IRF1 directly.…”

Section: Discussionmentioning

confidence: 90%

MicroRNA-23a-3p Down-Regulation in Active Pulmonary Tuberculosis Patients with High Bacterial Burden Inhibits Mononuclear Cell Function and Phagocytosis through TLR4/TNF-α/TGF-β1/IL-10 Signaling via Targeting IRF1/SP1

Chen

Lee

Hsiao

et al. 2020

IJMS

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The aim of this study is to explore the role of microRNAs (miR)-21/23a/146a/150/155 targeting the toll-like receptor pathway in active tuberculosis (TB) disease and latent TB infection (LTBI). Gene expression levels of the five miRs and predicted target genes were assessed in peripheral blood mononuclear cells from 46 patients with active pulmonary TB, 15 subjects with LTBI, and 17 non-infected healthy subjects (NIHS). THP-1 cell lines were transfected with miR-23a-3p mimics under stimuli with Mycobacterium TB-specific antigens. Both miR-155-5p and miR-150-5p gene expressions were decreased in the active TB group versus the NIHS group. Both miR-23a-3p and miR-146a-5p gene expressions were decreased in active TB patients with high bacterial burden versus those with low bacterial burden or control group (LTBI + NIHS). TLR2, TLR4, and interleukin (IL)10 gene expressions were all increased in active TB versus NIHS group. MiR-23a-3p mimic transfection reversed ESAT6-induced reduction of reactive oxygen species generation, and augmented ESAT6-induced late apoptosis and phagocytosis, in association with down-regulations of the predicted target genes, including tumor necrosis factor (TNF)-α, TLR4, TLR2, IL6, IL10, Notch1, IL6R, BCL2, TGF-β1, SP1, and IRF1. In conclusion, the down-regulation of miR-23a-3p in active TB patients with high bacterial burden inhibited mononuclear cell function and phagocytosis through TLR4/TNF-α/TGF-β1/IL-10 signaling via targeting IRF1/SP1.

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“…Previous studies have shown that the hyperglycemia environment in diabetic skin can enhance OS and increase the inflammatory response of keratinocytes, thus stagnating the wound-healing process in the inflammatory phase. 7,71,78 Studies have confirmed that miR-132 is the key miRNA that determines the transition from inflammation to proliferation in wounds. Both in vivo and in vitro experiments have confirmed that miR-132 knockout causes severe inflammation, inhibits keratinocyte proliferation, and delays wound healing.…”

Section: Anti-inflammatory Effectsmentioning

confidence: 98%

“…66 Similarly, miR-23a inhibited the expression of IRF-1 and reduced the expression of inducible nitric oxide synthase (iNOS) and the angiogenesis-related factor vascular endothelial growth factor (VEGF), thus inhibiting angiogenesis and the healing process of diabetic wounds. 78 Another study showed that miR-221-3p increased the expression of VEGF and promoted cell proliferation and angiogenesis. Bioinformatics analysis indicated that miR-221-3p may be involved in AGE-receptor for AGE (RAGE) signaling, cell cycle, and p53 signaling in diabetes.…”

Section: Angiogenesis Promotionmentioning

confidence: 99%

“…Downregulating the expression of miR-23a reduced its inhibitory effect on downstream gene IRF-1 and upregulated iNOS, promoted wound angiogenesis, and facilitated the healing of DFUs. 78 Sawaya et al 8 reported that the topical application of mevastatin accelerated wound healing; one of the possible mechanisms is that mevastatin induced the expression of lncRNA-Gas5. lncRNA-Gas5 inhibits the expression of the transcription factor c-Myc, which regulates the proliferation and migration of keratinocytes, thereby promoting wound healing.…”

Section: The Application Prospects Of Ncrna In Diagnosis and Treatmentmentioning

confidence: 99%

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The progress, prospects, and challenges of the use of non-coding RNA for diabetic wounds

Wei

Liu

et al. 2021

Molecular Therapy - Nucleic Acids

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Chronic diabetic wounds affect the quality of life of patients, resulting in significant social and economic burdens on both individuals and the health care system. Although treatment methods for chronic diabetic wounds have been explored, there remains a lack of effective treatment strategies; therefore, alternative strategies must be explored. Recently, the abnormal expression of non-coding RNA in diabetic wounds has received widespread attention since it is an important factor in the development of diabetic wounds. This article reviews the regulatory role of three common non-coding RNAs (microRNA [miRNA], long non-coding RNA [lncRNA], and circular RNA [circRNA]) in diabetic wounds and discusses the diagnosis, treatment potential, and challenges of non-coding RNA in diabetic wounds. This article provides insights into new strategies for diabetic wound diagnosis and treatment at the genetic and molecular levels. ncRNA ncRNA refers to a type of RNA that does not encode protein. In the past, it has been shown to participate in a variety of biological processes and play important transcriptional and post-transcriptional regulatory functions. 18 ncRNAs are divided into two categories based on the length of the RNA chain; lncRNA have lengths greater than 200 nucleotides, and small ncRNAs (snRNA) have lengths less than 200 nucleotides. snRNAs can be subdivided into miRNAs and circRNAs. 19 miRNAs inhibit the expression of target genes by binding to the 3 0 untranslated region (3 0 UTR) of the target mRNA. 20 The miRNA gene is processed and cleaved by RNA polymerase II (Pol II) enzyme and endonuclease Drosha III to produce pre-miRNA, which is

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Ginsenoside (Rg-1) promoted the wound closure of diabetic foot ulcer through iNOS elevation via miR-23a/IRF-1 axis

Cited by 42 publications

References 25 publications

Macrophage-derived exosomes accelerate wound healing through their anti-inflammation effects in a diabetic rat model

Macrophage-derived exosomes accelerate wound healing through their anti-inflammation effects in a diabetic rat model

MicroRNA-23a-3p Down-Regulation in Active Pulmonary Tuberculosis Patients with High Bacterial Burden Inhibits Mononuclear Cell Function and Phagocytosis through TLR4/TNF-α/TGF-β1/IL-10 Signaling via Targeting IRF1/SP1

The progress, prospects, and challenges of the use of non-coding RNA for diabetic wounds

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