MicroRNA-381 reduces inflammation and infiltration of macrophages in polymyositis via downregulating HMGB1

Liu, Yutao; Gao, Yuan; Yang, Jing; Shi, Changhe; Wang, Yanlin; Xu, Yuming

doi:10.3892/ijo.2018.4463

Cited by 15 publications

(14 citation statements)

References 50 publications

(52 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In VSMCs, HMGB1 is known to promote VSMC migration by activating the TLR4/PI3K/Akt pathway 31 and to facilitate smooth muscle cell proliferation by activating c‐Jun 32 . Previous studies report that miR‐381‐3p can repress the expression of inflammatory cytokines, such as TNF‐α and IL‐17, by regulating HMGB1, thereby attenuating the development of neuropathic pain and polymyositis 33,34 . Our data indicated that HMGB1 expression was observably increased in human VSMCs cultured in a high glucose environment, and it was repressed by miR‐381‐3p at the mRNA and protein levels.…”

Section: Discussionsupporting

confidence: 53%

miR‐381‐3p inhibits high glucose‐induced vascular smooth muscle cell proliferation and migration by targeting HMGB1

Zhu

Zhou

Yang

et al. 2020

The Journal of Gene Medicine

View full text Add to dashboard Cite

BackgroundHyperglycemia increases the risk of many cardiovascular diseases (CVD), and the dysregulation of proliferation and migration in vascular smooth muscle cells (VSMCs) also participates in the pathogenesis of CVD. miR‐381‐3p is known to suppress the proliferation and migration of multiple human cell types. Nevertheless, the function of miR‐381‐3p in VSMCs remains largely indistinct.MethodsA quantitative real‐time polymerase chain reaction (qRT‐PCR) was employed to investigate miR‐381‐3p expression in high‐glucose‐induced VSMCs. Inflammatory cytokines tumor necrosis factor‐α, interleukin‐1β and interleukin‐6, as well as oxidative stress markers SOD and MDA, were determined by an enzyme‐linked immunosorbent assay. Reactive oxygen species generation was examined using a 2,7'‐dichlorofluorescein kit. The proliferation, migration and apoptosis of VSMCs were monitored by 3‐(4,5‐dimethylthiazl2‐yl)‐2,5‐diphenyltetazolium bromide (MTT), transwell and terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling (TUNEL) assays. The TargetScan database (http://www.targetscan.org) was employed to seek the potential target gene of miR‐381‐3p. Interaction between miR‐381‐3p and HMGB1 was determined by a qRT‐PCR, western blotting and a luciferase reporter assay.ResultsmiR‐381‐3p expression was significantly reduced in a VSMCs dysfunction model induced by high‐glucose in a dose‐ and time‐dependent manner. Transfection of miR‐381‐3p mimics suppressed the inflammation, oxidative stress, proliferation and migration of VSMCs, whereas apoptosis of VSMCs was promoted, and the transfection of miR‐381‐3p inhibitors had the opposite effect. Mechanistically, HMGB1, an important factor in inflammation response, was confirmed as a target gene of miR‐381‐3p.ConclusionsmiR‐381‐3p targets HMGB1 to suppress the inflammation, oxidative stress, proliferation and migration of high‐glucose‐induced VSMCs by targeting HMGB1.

show abstract

Section: Discussionsupporting

confidence: 53%

miR‐381‐3p inhibits high glucose‐induced vascular smooth muscle cell proliferation and migration by targeting HMGB1

Zhu

Zhou

Yang

et al. 2020

The Journal of Gene Medicine

View full text Add to dashboard Cite

show abstract

“…a recent study demonstrated that overexpression of mir-381 in raW264.7 cell lines decreased the concentrations of il-1β and TnF-α (42). in addition, mir-381 can reduce inflammation and the infiltration of macrophages by targeting high-mobility group box 1 mrna (43). in addition, mir-381 can regulate notch signaling-mediated cardioprotective effect in cardiomyocytes (44).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of microRNA‑381 against inflammatory damage of endothelial cells during coronary heart disease by targeting CXCR4

Huang

Hong

et al. 2020

Mol Med Report

View full text Add to dashboard Cite

coronary heart disease (cHd) is the leading cause of human morbidity and mortality worldwide. Microrna (mirna) profiling is an innovative method of identifying biomarkers for many diseases and may be a powerful tool in the diagnosis and treatment of cHd. The present study aimed to analyze the effects of miRNA (miR)-381 on the inflammatory damage of endothelial cells during cHd. a total of 21 patients with cHd and 21 healthy control patients were enrolled in this study. reverse transcription-quantitative PCR, western blotting and immunofluorescence assays were conducted to examine the expression levels of mir-381, c-X-c chemokine receptor type 4 (cXcr4), Bcl-2, Bax, cleaved-caspases-3 and-9, p38, erK1/2 and JnK. cell Counting Kit-8, EdU and flow cytometry experiments were performed to evaluate cell proliferation and apoptosis. an ELISA was adopted to determine the expressions of inflammatory factors (interleukins-8,-6 and-1β, and tumor necrosis factor-α). in addition, a dual-luciferase reporter assay was used to determine the relationship between mir-381 and cXcr4. decreased mir-381 expression and increased cXcr4 expression in the plasma were observed in the cHd group compared with the normal group, which indicated a negative relationship between mir-381 and cXcr4. overexpression of mir-381 significantly promoted the proliferation and inhibited the apoptosis of oxidized low-density lipoprotein (oX-ldl)-induced human umbilical vein endothelial cells (HuVecs) through mitogen-activated protein kinase pathway by targeting and inhibiting cXcr4. Furthermore, overexpression of miR-381 reduced the release of inflammatory factors in oX-ldl-induced HuVecs. By contrast, reduced expression of mir-381 exerted the opposite effects, which were subsequently reversed by silencing cXcr4 expression. results from the present study indicated that mir-381 was a cHd-related factor that may serve as a potential molecular target for cHd treatment.

show abstract

“…It is very possible that downregulation of miR-206–3p by MDI exposure may cause upregulation of CCL2/MCP-1 through direct binding of miR-206–3p to the CCL2/MCP-1 3′UTR; further study of this phenomenon is needed. Recently, miR-381–3p has been shown to target the high mobility group box 1 (HMGB1) gene resulting in reduced macrophage mobility and infiltration in polymyositis (Liu et al, 2018). HMGB1 is a highly conserved DNA binding protein that is an important modulator of immune and inflammatory responses in airway inflammation (Yang et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Acute 4,4′-Methylene Diphenyl Diisocyanate Exposure-Mediated Downregulation of miR-206-3p and miR-381-3p Activates Inducible Nitric Oxide Synthase Transcription by Targeting Calcineurin/NFAT Signaling in Macrophages

Lin

Law

Hettick

2019

Toxicological Sciences

View full text Add to dashboard Cite

Exposure to 4,4′-methylene diphenyl diisocyanate (MDI) in the occupational setting may lead to development of occupational asthma (OA), and the underlying molecular mechanisms of MDI-induced disease pathogenesis remain an active area of research. Using a nose-only mouse inhalation model, we find that circulating microRNA (miR)-206–3p and miR-381–3p are downregulated after MDI exposure; however, cellular miR-206–3p and miR-381–3p responses after MDI aerosol exposure and their pathophysiological roles in MDI-OA are unknown. We hypothesize that miR-206–3p and miR-381–3p-regulated mechanisms cause increased expression of the inducible nitric oxide synthase (iNOS) after MDI aerosol exposure. We examined cellular miR-206–3p and miR-381–3p, calcineurins, nuclear factors of activated T cells (NFATs), and iNOS levels from both nose-only exposed murine bronchoalveolar lavage cells (BALCs) and differentiated THP-1 macrophages treated with MDI-glutathione (GSH) conjugates. Both in vivo murine MDI aerosol exposure and in vitro MDI-GSH exposures in THP-1 macrophages result in downregulation of endogenous miR-206–3p and miR-381–3p and upregulation of PPP3CA and iNOS expression. Transfection of THP-1 macrophages with miR-inhibitor-206–3p and miR-inhibitor-381–3p resulted in the upregulation of PPP3CA and iNOS. Using RNA-induced silencing complex immunoprecipitation and translational reporter assays, we verified that PPP3CA, but not iNOS, is directly targeted by both miR-206–3p and miR-381–3p. Downregulation of miR-206–3p and miR-381–3p following by MDI exposure induces calcineurin/NFAT signaling-mediated iNOS transcription in macrophages and BALCs.

show abstract

MicroRNA-381 reduces inflammation and infiltration of macrophages in polymyositis via downregulating HMGB1

Cited by 15 publications

References 50 publications

miR‐381‐3p inhibits high glucose‐induced vascular smooth muscle cell proliferation and migration by targeting HMGB1

miR‐381‐3p inhibits high glucose‐induced vascular smooth muscle cell proliferation and migration by targeting HMGB1

Protective effect of microRNA‑381 against inflammatory damage of endothelial cells during coronary heart disease by targeting CXCR4

Acute 4,4′-Methylene Diphenyl Diisocyanate Exposure-Mediated Downregulation of miR-206-3p and miR-381-3p Activates Inducible Nitric Oxide Synthase Transcription by Targeting Calcineurin/NFAT Signaling in Macrophages

Contact Info

Product

Resources

About