MicroRNA-24 inhibits the oxidative stress induced by vascular injury by activating the Nrf2/Ho-1 signaling pathway

Zhang, Jing; Cai, Wanyin; Fan, Zhixing; Yang, Chaojun; Wang, Wei; Xiong, Mingrui; Ma, Cong; Yang, Jian

doi:10.1016/j.atherosclerosis.2019.08.023

Cited by 48 publications

(46 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Reactive oxygen species (ROS) are produced in large quantities in skin wounds due to chronic in ammation, which will further aggravate the in ammatory response and toxic effects of cells [43].The reduction of antioxidant active substances such as superoxide dismutase (SOD) and glutathione peroxidase (GPx) and the increase of free radicals can all lead to delayed healing of diabetic wounds [44].This is consistent with our experimental results. Through extracorporeal experiments, we can nd that LPS-Exos can signi cantly reduce the reactive oxygen species induced by endothelial cells under high glucose treatment.At the same time, different concentrations of LPS-Exos can increase the antioxidant substances in the wounds of diabetic rats to different degrees.…”

Section: Discussionsupporting

confidence: 86%

LPS-stimulated Macrophage Exosomes Inhibit Inflammation by Activating the Nrf2 / HO-1 Defense Pathway and Promote Wound Healing in Diabetic Rats

Tian

et al. 2020

Preprint

View full text Add to dashboard Cite

Background:Impaired wound healing is one of the important complications of diabetes. However, the specific pathogenesis is still unclear, and there is no effective treatment. Macrophages pretreated with chemical or biological factors may increase the biological activity of macrophage-derived exosomes, which is expected to become a new effective treatment method. The purpose of this study was to investigate whether the exosomes secreted by macrophages pretreated with lipopolysaccharide (LPS) have better anti-inflammatory and angiogenic abilities in the treatment of diabetic wound healing and their underlying molecular mechanisms.Methods:In this study, macroscopical, biochemical, histological, immunofluorescence and molecular biology methods were used to evaluate the potential protective mechanism and effect of lipopolysaccharide stimulated macrophage exosomes (LPS-Exos) on wound healing in streptozotocin induced hyperglycemia rats.In the in vivo experiment, the percentages of wound closure and contraction were compared and analyzed on the 7th, 14th, and 21st day after treatment by grouping treatments with different concentrations of LPS-Exos.At the same time, hematoxylin and eosin staining (HE), Masson staining, immunofluorescence staining and Western blotting (WB) were used for histological analysis of the wound tissue on the 14th day after injury to evaluate the impact of different treatment methods on wound healing.In in vitro experiments, the ability of endothelial cells related to proliferation, migration, tube formation and the expression of vascular endothelial growth factor (VEGF) were tested.At the same time, in vivo and in vitro experiments, the effect of Nrf2/HO-1 signaling pathway on LPS-Exos in inhibiting inflammation and promoting angiogenesis was evaluated by using exosome-specific inhibitors.Results:LPS-Exos reduced the content of ROS and MDA in the wound tissue of hyperglycemic rats, increased the activity of SOD and the production of GSH-Px, activated the Nrf2/HO-1 pathway, inhibited the expression of inflammation-related proteins, and promoted blood vessels generate. The group given exosome inhibitors reversed this phenomenon.Conclusions: LPS-Exos may activate the Nrf2/HO-1 defense pathway, improve endothelial cell function, inhibit oxidative damage and inflammation, and promote wound healing in diabetic rats, thereby having the potential to treat diabetic skin defects.

show abstract

Section: Discussionsupporting

confidence: 86%

LPS-stimulated Macrophage Exosomes Inhibit Inflammation by Activating the Nrf2 / HO-1 Defense Pathway and Promote Wound Healing in Diabetic Rats

Tian

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…The delay in endothelialization severely compromises the therapeutic effect of Ecs (40). Previously published data by the authors of the current study demonstrated that miR-24 was enriched in VSMcs rather than Ecs (41). The present study demonstrated that miR-24 gene transfer increased cd31 expression and accelerated reendothelialization following arterial injury in diabetic rats.…”

Section: Discussionsupporting

confidence: 49%

MicroRNA‑24 attenuates diabetic vascular remodeling by�suppressing the NLRP3/caspase‑1/IL‑1β signaling pathway

Fan

Yang

et al. 2020

Int J Mol Med

Self Cite

View full text Add to dashboard Cite

Vascular remodeling plays an important role in the pathogenesis of diabetic cardiovascular complications. Previous published research has indicated that microRNA-24 (miR-24) is involved in diabetic vascular remodeling, but the underlying molecular mechanisms have yet to be fully elucidated. The aim of the present study was to investigate whether adenovirus-mediated miR-24 overexpression can suppress the NOd-like receptor family pyrin domain-containing 3 (NLRP3)-related inflammatory signaling pathway and attenuate diabetic vascular remodeling. The carotid arteries of diabetic rats were harvested and prepared for analysis. Reverse transcription-quantitative PcR and western blotting assays were used to detect the expressions of related mRNAs and proteins. Morphological examinations, including hematoxylin and eosin, immunohistochemical and Masson's trichrome staining, were also performed. The results of the present study demonstrated that miR-24 upregulation suppressed neointimal hyperplasia and accelerated reendothelialization in the injured arteries, lowered the expression of NLRP3, apoptosis-associated speck-like protein, caspase-1, proliferating cell nuclear antigen, cd45, interleukin (IL)-1β, IL-18 and tumor necrosis factor-α, and increased the expression of cd31, smooth muscle (SM) α-actin and SM-myosin heavy chain. These data indicated that miR-24 overexpression can attenuate vascular remodeling in a diabetic rat model through suppressing the NLRP3/caspase-1/IL-1β signaling pathway.

show abstract

“…In this case, miRNA-24 regulated the Nrf2/HO-1 signaling pathway indirectly by regulating of Keap1 after influencing of O-linked β-N-acetylglucosamine transferase gene (Ogt). On the other hand, authors confirmed that miRNA-24 affects the expression of SOD, malondialdehyde, and glutathione peroxidase [137].…”

Section: Coronary Artery Diseases (Cad)mentioning

confidence: 89%

“…Endothelial cell apoptosis under oxidative stress plays a critical role in the initiation and progression of atherosclerosis [131][132][133][134][135][136][137][138][139][140][141]. Li et al observed that overexpression of miRNA-210 caused inhibition of apoptosis and reduction of ROS level in human umbilical vein endothelial cells (HUVECs) treated with H 2 O 2 and also downregulation of caspase levels.…”

Section: Coronary Artery Diseases (Cad)mentioning

confidence: 99%

“…MiRNA-24 is highly expressed in the vessel wall and changes of its expression are connected with dysfunction and injury of vascular endothelial cells [132]. It is believed that miRNA-24 participates in many pathophysiological processes including I/R injury or vascular oxidative stress [134][135][136][137]. In an experimental study by Zhang et al, miRNA-24 was upregulated, and it has a supportive effect on vascular endothelium repair by attenuating oxidative-stress-induced damage of endothelial cells.…”

Section: Coronary Artery Diseases (Cad)mentioning

confidence: 99%

See 1 more Smart Citation

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Kura

Bačová

Kaločayová

et al. 2020

IJMS

125

View full text Add to dashboard Cite

Reactive oxygen species (ROS) are important molecules in the living organisms as a part of many signaling pathways. However, if overproduced, they also play a significant role in the development of cardiovascular diseases, such as arrhythmia, cardiomyopathy, ischemia/reperfusion injury (e.g., myocardial infarction and heart transplantation), and heart failure. As a result of oxidative stress action, apoptosis, hypertrophy, and fibrosis may occur. MicroRNAs (miRNAs) represent important endogenous nucleotides that regulate many biological processes, including those involved in heart damage caused by oxidative stress. Oxidative stress can alter the expression level of many miRNAs. These changes in miRNA expression occur mainly via modulation of nuclear factor erythroid 2-related factor 2 (Nrf2), sirtuins, calcineurin/nuclear factor of activated T cell (NFAT), or nuclear factor kappa B (NF-κB) pathways. Up until now, several circulating miRNAs have been reported to be potential biomarkers of ROS-related cardiac diseases, including myocardial infarction, hypertrophy, ischemia/reperfusion, and heart failure, such as miRNA-499, miRNA-199, miRNA-21, miRNA-144, miRNA-208a, miRNA-34a, etc. On the other hand, a lot of studies are aimed at using miRNAs for therapeutic purposes. This review points to the need for studying the role of redox-sensitive miRNAs, to identify more effective biomarkers and develop better therapeutic targets for oxidative-stress-related heart diseases.

show abstract

MicroRNA-24 inhibits the oxidative stress induced by vascular injury by activating the Nrf2/Ho-1 signaling pathway

Cited by 48 publications

References 62 publications

LPS-stimulated Macrophage Exosomes Inhibit Inflammation by Activating the Nrf2 / HO-1 Defense Pathway and Promote Wound Healing in Diabetic Rats

LPS-stimulated Macrophage Exosomes Inhibit Inflammation by Activating the Nrf2 / HO-1 Defense Pathway and Promote Wound Healing in Diabetic Rats

MicroRNA‑24 attenuates diabetic vascular remodeling by�suppressing the NLRP3/caspase‑1/IL‑1β signaling pathway

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Contact Info

Product

Resources

About

MicroRNA-24 inhibits the oxidative stress induced by vascular injury by activating the Nrf2/Ho-1 signaling pathway

Cited by 48 publications

References 62 publications

LPS-stimulated Macrophage Exosomes Inhibit Inflammation by Activating the Nrf2&nbsp;/ HO-1 Defense Pathway and Promote Wound Healing in Diabetic Rats

LPS-stimulated Macrophage Exosomes Inhibit Inflammation by Activating the Nrf2&nbsp;/ HO-1 Defense Pathway and Promote Wound Healing in Diabetic Rats

MicroRNA‑24 attenuates diabetic vascular remodeling by�suppressing the NLRP3/caspase‑1/IL‑1β signaling pathway

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Contact Info

Product

Resources

About

LPS-stimulated Macrophage Exosomes Inhibit Inflammation by Activating the Nrf2 / HO-1 Defense Pathway and Promote Wound Healing in Diabetic Rats

LPS-stimulated Macrophage Exosomes Inhibit Inflammation by Activating the Nrf2 / HO-1 Defense Pathway and Promote Wound Healing in Diabetic Rats