miR-5591-5p regulates the effect of ADSCs in repairing diabetic wound via targeting AGEs/AGER/JNK signaling axis

Li, Qiang; Xia, Sizhan; Yin, Yating; Guo, Yanping; Chen, Feifei; Jin, Peisheng

doi:10.1038/s41419-018-0615-9

Cited by 30 publications

(39 citation statements)

References 38 publications

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“…All the methods were carried out as described in previous studies [ 18 – 20 ]. Adipose tissue samples were obtained from three liposuction aspirates of patients (age range 30–45 years) with informed consent at the Affiliated Hospital of Xuzhou Medical University.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of autophagy promoted high glucose/ROS-mediated apoptosis in ADSCs

Yin

Zheng

et al. 2018

Stem Cell Res Ther

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BackgroundIncreased apoptosis in adipose tissue-derived stem cells (ADSCs) limits their application in treating diabetes complications. Autophagy is a molecular process that allows cells to degrade and recover damaged macromolecules, and closely interacts with apoptosis. The aim of the present study was to investigate the potential role of autophagy in ADSC apoptosis induced by high glucose.MethodsHuman ADSCs were cultured in normal or high-glucose medium for 6 h, 12 h, or 24 h. The effects of high glucose on ADSC autophagy, reactive oxygen species (ROS) production, and apoptosis were evaluated. The impact of autophagy on ROS production and apoptosis was explored by treatment with rapamycin or 3-methyladenine (3-MA). The c-jun kinase (JNK) signaling pathway was investigated by pharmacological disruption of SP600125.ResultsADSCs subjected to high glucose stress showed an obvious induction of autophagy and apoptosis and a significant increase in intracellular ROS levels. The JNK signaling pathway was confirmed to be involved in high glucose-induced autophagy. Pre-treatment with SP600125 or N-acetylcysteine reversed the effects of high glucose on the JNK signaling pathway and autophagy-related proteins. Pretreatment of ADSCs with 3-MA under high glucose stress induced a further increase in ROS levels compared to those of high glucose-treated cells. Furthermore, ADSCs pretreated with 3-MA under high glucose stress showed a marked increase in apoptosis compared with that of the cells treated with high glucose. Conversely, pre-treatment with rapamycin inhibited the apoptosis of ADSCs.ConclusionsTaken together, our data suggest that autophagy may play a protective role in high glucose-induced apoptosis in ADSCs. ROS/JNK signaling is essential in upregulating high glucose-induced autophagy. This study provides new insights into the molecular mechanism of autophagy involved in high glucose-induced apoptosis in ADSCs.Electronic supplementary materialThe online version of this article (10.1186/s13287-018-1029-4) contains supplementary material, which is available to authorized users.

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Section: Methodsmentioning

confidence: 99%

Inhibition of autophagy promoted high glucose/ROS-mediated apoptosis in ADSCs

Yin

Zheng

et al. 2018

Stem Cell Res Ther

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“…A different approach to modulate RAGE signaling may be via microRNAs, some of which are being developed as potential therapeutics. For example, miR-5591–5p is downregulated by RAGE signaling and promoted cell survival and repair when overexpressed [116]. Another microRNA that is downregulated by AGEs, miR-126 is a negative regulator of IL-6 and TNF-α and prevents ROS and inflammation [117].…”

Section: Pharmaceutical Treatment Of Age Accumulationmentioning

confidence: 99%

Mechanistic targeting of advanced glycation end-products in age-related diseases

Rowan

Bejarano

Taylor

2018

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

167

125

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Glycative stress, caused by the accumulation of cytotoxic and irreversibly-formed sugar-derived advanced glycation end-products (AGEs), contributes to morbidity associated with aging, age-related diseases, and metabolic diseases. In this review, we summarize pathways leading to formation of AGEs, largely from sugars and glycolytic intermediates, and discuss detoxification of AGE precursors, including the glyoxalase system and DJ-1/Park7 deglycase. Disease pathogenesis downstream of AGE accumulation can be cell autonomous due to aggregation of glycated proteins and impaired protein function, which occurs in ocular cataracts. Extracellular AGEs also activate RAGE signaling, leading to oxidative stress, inflammation, and leukostasis in diabetic complications such as diabetic retinopathy. Pharmaceutical agents have been tested in animal models and clinically to diminish glycative burden. We summarize existing strategies and point out several new directions to diminish glycative stress including: plant-derived polyphenols as AGE inhibitors and glyoxalase inducers; improved dietary patterns, particularly Mediterranean and low glycemic diets; and enhancing proteolytic capacities of the ubiquitin-proteasome and autophagy pathways that are involved in cellular clearing of AGEs.

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“…MiRNAs control gene expression at the post-transcriptional and translational levels by binding to complementary sequences in the 3′-UTRs of target mRNAs (Li et al, 2018). We explored the underlying mechanisms and the correlations between miRNA-181a and caprin-1 in GC cells.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-181a Functions as an Oncogene in Gastric Cancer by Targeting Caprin-1

et al. 2019

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MicroRNA-181a (miRNA-181a) is a multifaceted miRNA implicated in various cellular processes, particularly in cell fate determination and cellular invasion. It is frequently expressed aberrantly in human tumors and shows opposing functions in different types of cancers. In this study, we found that miRNA-181a is overexpressed in Gastric cancer (GC) tissues. Clinical and pathological analyses revealed that the expression of miRNA-181a is correlated with tumor size, lymph node metastasis, distant metastasis, and TNM stage. Kaplan-Meier analysis indicated that overexpression of miRNA-181a is associated with poor overall survival of patients with GC. Moreover, miRNA-181a is overexpressed in GC cells, and downregulation of miRNA-181a induced cell apoptosis and suppressed the proliferation, invasion, and metastasis of GC cells both in vitro and in vivo. Target prediction and luciferase reporter assay showed that caprin-1 was a direct target of miRNA-181a. Downregulation of caprin-1 expression resulted in a converse change with miRNA-181a in GC. Spearman’s correlation test confirmed that the expression of miRNA-181a expression was inversely correlated with that of caprin-1 in GC cells. Furthermore, the expression of caprin-1 increased after downregulation of miRNA-181a in the GC cells. Caprin-1 siRNA can rescue the oncogenic effect of miRNA-181a on GC cell proliferation, apoptosis, migration, and invasion. These findings suggest that miRNA-181a directly inhibits caprin-1 and promotes GC development. miRNA-181a could be a target for anticancer drug development.

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miR-5591-5p regulates the effect of ADSCs in repairing diabetic wound via targeting AGEs/AGER/JNK signaling axis

Cited by 30 publications

References 38 publications

Inhibition of autophagy promoted high glucose/ROS-mediated apoptosis in ADSCs

Inhibition of autophagy promoted high glucose/ROS-mediated apoptosis in ADSCs

Mechanistic targeting of advanced glycation end-products in age-related diseases

MicroRNA-181a Functions as an Oncogene in Gastric Cancer by Targeting Caprin-1

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