MiR-506-3p regulates autophagy and proliferation in post-burn skin fibroblasts through post-transcriptionally suppressing Beclin-1 expression

Shi, Min; Zong, Xiaoming; Chen, Lei; Guo, Xinfeng; Ding, Xuanfeng

doi:10.1007/s11626-020-00472-3

Cited by 9 publications

(6 citation statements)

References 45 publications

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“…Therefore, the application of these autophagy regulators is still limited in the clinical setting. Additionally, monotropein (a bioactive constitutional used in traditional Chinese medicine) and noncoding RNA have also been confirmed to promote wound healing by regulating autophagy [ 97 , 98 ]. Moreover, MSCs have shown promising results for repairing damaged tissues both in animal models and in human clinical trials and may become an ideal autophagy inducer in the promotion of wound healing [ 83 ].…”

Section: Reviewmentioning

confidence: 99%

Autophagy and skin wound healing

et al. 2022

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Autophagy is a lysosome-dependent, self-renewal mechanism that can degrade and recycle cellular components in eukaryotic cells to maintain the stability of the intracellular environment and the cells ability to cope with unfavorable environments. Numerous studies suggest that autophagy participates in regulating various cellular functions and is closely associated with the onset and progression of various diseases. Wound healing is a complex, multistep biological process that involves multiple cell types. Refractory wounds, which include diabetic skin ulcers, can seriously endanger human health. Previous studies have confirmed that autophagy plays an essential role in various phases of wound healing. Specifically, in the inflammatory phase, autophagy has an anti-infection effect and it negatively regulates the inflammatory response, which prevents excessive inflammation from causing tissue damage. In the proliferative phase, local hypoxia in the wound can induce autophagy, which plays a role in anti-apoptosis and anti-oxidative stress and promotes cell survival. Autophagy of vascular endothelial cells promotes wound angiogenesis and that of keratinocytes promotes their differentiation, proliferation and migration, which is conducive to the completion of wound re-epithelialisation. In the remodeling phase, autophagy of fibroblasts affects the formation of hypertrophic scars. Additionally, a refractory diabetic wound may be associated with increased levels of autophagy, and the regulation of mesenchymal stem cell autophagy may improve its application to wound healing. Therefore, understanding the relationship between autophagy and skin wound healing and exploring the molecular mechanism of autophagy regulation may provide novel strategies for the clinical treatment of wound healing.

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Section: Reviewmentioning

confidence: 99%

Autophagy and skin wound healing

et al. 2022

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“…[15][16][17] This review will only include previous human research. Samples used to study burn-related miRNAs include adult skin fibroblasts, [18][19][20][21] skin epidermal stem cells, 22 skin, [23][24][25][26][27] wound tissues 28,29 and hypertrophic scar (HS) tissues. [30][31][32][33] Samples used to study wound-healing related miRNAs include healthy skin, [34][35][36] chronic non-healing ulcer tissue, 37,38 epidermal keratinocytes 39 and the HaCaT cell line.…”

Section: Samples Used To Identify Mirnas Involved In Burn Wound Heali...mentioning

confidence: 99%

“…Other techniques include microarrays (miRCURY LNA, Affymetrix GeneChip, and Agilent) and high throughput sequencing. Although qRT-PCR is the most commonly used technique, only 58 miRNAs were identified in the 27 articles that utilised the technique, [18][19][20][21][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][45][46][47][48][49][50] while the expression level of 82 miRNAs were measured by sequencing in two research studies. 22,38 In comparison, alterations in the expression of 203 miRNAs were detected using three different microarrays in seven research studies.…”

Section: Techniques Used To Measure Mirna Expressionmentioning

confidence: 99%

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MicroRNAs involved in human skin burns, wound healing and scarring

Siu

Voisey²,

Zang

et al. 2023

Wound Repair Regeneration

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MicroRNAs are small, non‐coding RNAs that regulate gene expression, and consequently protein synthesis. Downregulation and upregulation of miRNAs and their corresponding genes can alter cell apoptosis, proliferation, migration and fibroproliferative responses following a thermal injury. This review summarises the evidence for altered human miRNA expression post‐burn, and during wound healing and scarring. In addition, the most relevant miRNA targets and their roles in potential pathways are described. Previous studies using molecular techniques have identified 197 miRNAs associated with human wound healing, burn wound healing and scarring. Five miRNAs alter the expression of fibroproliferative markers, proliferation and migration of fibroblasts and keratinocytes post‐burn: hsa‐miR‐21 and hsa‐miR‐31 are increased after wounding, and hsa‐miR‐23b, hsa‐miR‐200b and hsa‐let‐7c are decreased. Four of these five miRNAs are associated with the TGF‐β pathway. In the future, large scale, in vivo, longitudinal human studies utilising a range of cell types, ethnicity and clinical healing outcomes are fundamental to identify burn wound healing and scarring specific markers. A comprehensive understanding of the underlying pathways will facilitate the development of clinical diagnostic or prognostic tools for better scar management and the identification of novel treatment targets for improved healing outcomes in burn patients.

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“…Notably, recent studies have shown that there are still some other micro RNAs that are related to the occurrence of keloid (Table 4). 82–96 Zhang et al suggested miR‐637 participated in the keloid progression by inhibition of Smad3 by comparing normal and keloid tissue 82 . Through Ingenol Mebutate inducing DNA damage, De et al found miR‐34a could regulate cell‐cycle progression and apoptosis together with p53, indicating miR‐34 plays a key role in keloid formation 83 .…”

Section: Epigeneticmentioning

confidence: 99%

Keloid: Genetic susceptibility and contributions of genetics and epigenetics to its pathogenesis

Liu

Yang

Song

et al. 2022

Experimental Dermatology

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Keloid, characterized by fibroproliferative disorders of the skin, can be developed in people of different genders, ages and ethnicities. Keloid can appear in any part of the body but are especially common on the earlobe, upper torso and triangular muscle. The genetic heterogeneity and susceptibility of KD (keloid) vary among different races and ethnicities. Studies have found that multiple loci on multiple chromosomes are associated with the pathogenesis of KD, and specific gene variants may also be involved. Despite multiple investigations attempting to uncover the aetiology of keloid formation, the genetic mechanism of keloid formation remains unknown. To establish a foundation for a better understanding of the genetics and epigenetics of keloids, we have evaluated and summarized current studies which are mostly related to heredity, genetic polymorphisms, predisposing gene, DNA methylation and non‐coding RNA. We also discussed the problems and potential of genetic and epigenetic investigations of keloids, with the goal of developing new therapeutic approaches to enhance the prognosis of keloid patients.

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MiR-506-3p regulates autophagy and proliferation in post-burn skin fibroblasts through post-transcriptionally suppressing Beclin-1 expression

Cited by 9 publications

References 45 publications

Autophagy and skin wound healing

Autophagy and skin wound healing

MicroRNAs involved in human skin burns, wound healing and scarring

Keloid: Genetic susceptibility and contributions of genetics and epigenetics to its pathogenesis

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