MicroRNA 199a-5p induces apoptosis by targeting JunB

Yan, Mengjie; Yang, Sibao; Meng, F.; Zhao, Zhihui; Zhong, Tian; Yang, Ping

doi:10.1038/s41598-018-24932-9

Cited by 38 publications

(36 citation statements)

References 34 publications

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“…NFKBIA played protective roles in myocardial injury by relieving inflammation through the inhibition of the NF‐κB signalling pathway (Figure 2). In addition, the information retrieval of these 4 genes in MI revealed that the involvement of CXCL8, CD44 and JUNB in the functional mechanism of MI has been reported, while few reports have investigated the role of NFKBIA in MI. Additionally, as NFKBIA was crucially involved in the NF‐κB signalling pathway, further investigations on NFKBIA are needed to acquire further insight into the functional mechanism of the NF‐κB signalling pathway in MI.…”

Section: Resultsmentioning

confidence: 99%

Silencing of ATP2B1‐AS1 contributes to protection against myocardial infarction in mouse via blocking NFKBIA‐mediated NF‐κB signalling pathway

Song

Zhang

et al. 2020

J Cellular Molecular Medi

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Myocardial infarction (MI) is an acute coronary syndrome that refers to tissue infarction of the myocardium. This study aimed to investigate the effect of long intergenic non-protein-coding RNA (lincRNA) ATPase plasma membrane Ca 2+ transporting 1 antisense RNA 1 (ATP2B1-AS1) against MI by targeting nuclear factor-kappa-B inhibitor alpha (NFKBIA) and mediating the nuclear factor-kappa-B (NF-κB) signalling pathway. An MI mouse model was established and identified by cardiac function evaluation. It was determined that ATP2B1-AS1 was highly expressed, while NFKBIA was poorly expressed and NF-κB signalling pathway was activated in MI mice. Cardiomyocytes were extracted from mice and introduced with a series of mouse ATP2B1-AS1 vector, NFKBIA vector, siRNA-mouse ATP2B1-AS1 and siRNA-NFKBIA. The expression of NF-κBp50, NF-κBp65 and IKKβ was determined to identify whether ATP2B1-AS1 and NFKBIA affect the NF-κB signalling pathway, the results of which suggested that ATP2B1-AS1 down-regulated the expression of NFKBIA and activated the NF-κB signalling pathway in MI mice. Based on the data from assessment of cell viability, cell cycle, apoptosis and levels of inflammatory cytokines, either silencing of mouse ATP2B1-AS1 or overexpression of NFKBIA was suggested to result in reduced cardiomyocyte apoptosis and expression of inflammatory cytokines, as well as enhanced cardiomyocyte viability. Our study provided evidence that mouse ATP2B1-AS1 silencing may have the potency to protect against MI in mice through inhibiting cardiomyocyte apoptosis and inflammation, highlighting a great promise as a novel therapeutic target for MI. K E Y W O R D Smouse ATPase plasma membrane Ca 2+ transporting 1 antisense RNA 1, myocardial infarction, NF-kappa-B inhibitor alpha, nuclear factor-kappa-B signalling pathway | INTRODUC TI ONMyocardial infarction (MI) is a major public health concern that is commonly known as a heart attack characterized by a decline or complete stop of blood flow to the heart. 1 Since 1998, age-standardized AMI incidence decreased from 323 to 210 per 100 000 in 2007 in female and from 620 to 380 per 100 000 in 2007 in male, but socio-economic inequalities still exist in AMI incidence and have not narrowed. 2 In America, more than one million patients are | 4467 SONG et al.hospitalized due to MI annually, and the rates of readmission are approximately 20% within 30 days after discharge. 3 Moreover, the incidence of MI is increasing in China, and 23 million patients are estimated to experience MI by the end of 2030. 4 The risk factors of MI include hypertension, hypercholesterolaemia, diabetes, smoking habit, obesity, a sedentary lifestyle, excessive alcohol intake and unhealthy diet. 5,6 Earlier recognition or diagnosis of MI symptoms and prompt care-seeking actions are of great significance for the selection of the most appropriate treatments. 7 Although great improvements have been achieved in the prevention and therapies of MI, the difficulties in the prevention of MI are still steadily increasing. 8 Thus, further ef...

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Section: Resultsmentioning

confidence: 99%

Silencing of ATP2B1‐AS1 contributes to protection against myocardial infarction in mouse via blocking NFKBIA‐mediated NF‐κB signalling pathway

Song

Zhang

et al. 2020

J Cellular Molecular Medi

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“…We found that JUN proto-oncogene (JUN) is a key TF-modulating interconnector for other TFs ( Figure 15D). Levels of JunB are reduced in association with apoptosis in cultured cells [111].…”

Section: Transcriptional Regulation Is Impaired By Ptnpsmentioning

confidence: 96%

“…Figure 1B shows that crystalline PtNPs had the features of a Pt face-centered cubic (fcc) phase. First (111), second (200), and third (220) peaks corresponded to 2θ values of 41.9 • , 46.5 • , and 67.5 • , respectively. The X-ray diffraction (XRD) peaks of PtNPs were broad and comparable to those of the corresponding bulk Pt material.…”

Section: Synthesis and Characterization Of Ptnps Using Lycopenementioning

confidence: 98%

Anisotropic Platinum Nanoparticle-Induced Cytotoxicity, Apoptosis, Inflammatory Response, and Transcriptomic and Molecular Pathways in Human Acute Monocytic Leukemia Cells

Gurunathan

Jeyaraj

et al. 2020

IJMS

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The thermoplasmonic properties of platinum nanoparticles (PtNPs) render them desirable for use in diagnosis, detection, therapy, and surgery. However, their toxicological effects and impact at the molecular level remain obscure. Nanotoxicology is mainly focused on the interactions of nanostructures with biological systems, particularly with an emphasis on elucidating the relationship between the physical and chemical properties such as size and shape. Therefore, we hypothesized whether these unique anisotropic nanoparticles could induce cytotoxicity similar to that of spherical nanoparticles and the mechanism involved. Thus, we synthesized unique and distinct anisotropic PtNPs using lycopene as a biological template and investigated their biological activities in model human acute monocytic leukemia (THP-1) macrophages. Exposure to PtNPs for 24 h dose-dependently decreased cell viability and proliferation. Levels of the cytotoxic markers lactate dehydrogenase and intracellular protease significantly and dose-dependently increased with PtNP concentration. Furthermore, cells incubated with PtNPs dose-dependently produced oxidative stress markers including reactive oxygen species (ROS), malondialdehyde, nitric oxide, and carbonylated protein. An imbalance in pro-oxidants and antioxidants was confirmed by significant decreases in reduced glutathione, thioredoxin, superoxide dismutase, and catalase levels against oxidative stress. The cell death mechanism was confirmed by mitochondrial dysfunction and decreased ATP levels, mitochondrial copy numbers, and PGC-1α expression. To further substantiate the mechanism of cell death mediated by endoplasmic reticulum stress (ERS), we determined the expression of the inositol-requiring enzyme (IRE1), (PKR-like ER kinase) PERK, activating transcription factor 6 (ATF6), and activating transcription factor 4 ATF4, the apoptotic markers p53, Bax, and caspase 3, and the anti-apoptotic marker Bcl-2. PtNPs could activate ERS and apoptosis mediated by mitochondria. A proinflammatory response to PtNPs was confirmed by significant upregulation of interleukin-1-beta (IL-1β), interferon γ (IFNγ), tumor necrosis factor alpha (TNFα), and interleukin (IL-6). Transcriptomic and molecular pathway analyses of THP-1 cells incubated with the half maximal inhibitory concentration (IC50) of PtNPs revealed the altered expression of genes involved in protein misfolding, mitochondrial function, protein synthesis, inflammatory responses, and transcription regulation. We applied transcriptomic analyses to investigate anisotropic PtNP-induced toxicity for further mechanistic studies. Isotropic nanoparticles are specifically used to inhibit non-specific cellular uptake, leading to enhanced in vivo bio-distribution and increased targeting capabilities due to the higher radius of curvature. These characteristics of anisotropic nanoparticles could enable the technology as an attractive platform for nanomedicine in biomedical applications.

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“…As the key regulator in the Wnt signaling pathway, miR-199a-5p induced muscle proliferation by targeting HIF-1, which is the key regulator in smooth muscle hypertrophy [36]. It also regulates cardiomyocyte apoptosis by targeting JunB (JunB proto-oncogene) [37]. In diabetic individuals, miR-199a-5p may be involved in skeletal muscle insulin resistance by inhibiting glucose transporter 4 (GLUT4) and hexokinase 2 (HK2) [38].…”

Section: Discussionmentioning

confidence: 99%

LncRNA IMFlnc1 Promotes Porcine Intramuscular Adipocyte Adipogenesis by Sponging Mir-199a-5p to Up-regulate CAV-1

Wang

Chen

et al. 2020

Preprint

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Background: Local Chinese local pig breeds have thinner muscle fiber and higher intramuscular-fat (IMF) content. But its regulation mechanism has not been discussed in-depth. Studies indicated that long non coding RNAs (lncRNAs) play important role in muscle and fat development.Results: The lncRNAs expressional differences in the longissimus dorsi (LD) muscle were identified between Huainan pigs (local Chinese pigs, fat-type, HN) and Large White pigs (lean-type, LW) at 38, 58, and 78 days post conception (dpc). In total, 2131 novel lncRNAs were identified in 18 samples, and 291, 305, and 683 differentially expressed lncRNAs (DELs) were found between these two breeds at three stages, respectively. GO and KEGG analysis of the DEL co expressed mRNAs showed that muscle development and energy metabolism were more active at 58 dpc in HN, but at 78 dpc in LW pigs. Muscle cell differentiation and myofibril assembly might associated with earlier myogenesis and primary-muscle-fiber assembly in HN, and cell proliferation, insulin, and the MAPK pathway might contribute to longer proliferation in LW pigs. The PI3K/Akt and cAMP pathways were associated with higher IMF deposition in HN. IMFlnc1 was selected for functional verification, and results indicated that it regulated the expressional level of caveolin-1 (CAV-1) by acting as competing endogenous RNA (ceRNA) to sponge miR-199a-5p.Conclusions: Our data contributed to understanding lncRNAs in porcine-muscle development and IMF deposition, and provided valuable information for improving pig-meat quality.

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MicroRNA 199a-5p induces apoptosis by targeting JunB

Cited by 38 publications

References 34 publications

Silencing of ATP2B1‐AS1 contributes to protection against myocardial infarction in mouse via blocking NFKBIA‐mediated NF‐κB signalling pathway

Silencing of ATP2B1‐AS1 contributes to protection against myocardial infarction in mouse via blocking NFKBIA‐mediated NF‐κB signalling pathway

Anisotropic Platinum Nanoparticle-Induced Cytotoxicity, Apoptosis, Inflammatory Response, and Transcriptomic and Molecular Pathways in Human Acute Monocytic Leukemia Cells

LncRNA IMFlnc1 Promotes Porcine Intramuscular Adipocyte Adipogenesis by Sponging Mir-199a-5p to Up-regulate CAV-1

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