Downregulation of microRNA-155 ameliorates high glucose-induced endothelial injury by inhibiting NF-κB activation and promoting HO-1 and NO production

Zhang, Xi; Li, Xiangyang; Li, Yang; Lai, Jingbo; Zhang, Nana; Ming, Jie; Ma, Xianjie; Ji, Qiuhe; Xing, Ying

doi:10.1016/j.biopha.2017.01.122

Cited by 9 publications

(7 citation statements)

References 49 publications

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“…A previous study revealed that ROS is associated with the initiation and progression stages of atherogenesis (25). Therefore, the present study investigated the effects of miR-34a on ROS induced by ox-LdL in HUVEcs.…”

Section: Knockdown Of Mir-34a Protects Against Ox-ldl-induced Rosmentioning

confidence: 87%

“…As a model for investigations involving Ecs, HUVEcs (HUVEc-cS) are widely used in the investigation of atherosclerosis (18,24,25). To investigate the effect of miR-34a on the development of atherosclerosis, the HUVEc model was established, which was treated with different concentrations (10-200 µg/ml) of ox-LdL for 24 h, and the level of miR-34a was measured using RT-qPCR analysis.…”

Section: Knockdown Of Mir-34a Prevents Ox-ldl-induced Huvec Apoptosismentioning

confidence: 99%

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Downregulation of microRNA‑34a inhibits oxidized low‑density lipoprotein‑induced apoptosis and oxidative stress in human umbilical vein endothelial cells

Zhang

et al. 2018

Int J Mol Med

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Oxidized low‑density lipoprotein (ox‑LDL) promotes endothelial cell dysfunction, which is a primary risk factor for the development of atherosclerosis. A previous study reported that microRNA (miRNA/miR)‑34a is upregulated in atherosclerotic samples. However, its function and underlying mechanisms remain to be fully elucidated. In the present study, miRNA microarray analysis was performed to investigate the miRNA expression profile in atherosclerotic plaque tissues and examine the role of miR‑34a in ox‑LDL‑induced apoptosis of human umbilical vein endothelial cells (HUVECs). Cell viability, apoptosis and protein expression was determined by a cell counting kit‑8 assay, flow cytometry and western blot analysis, respectively. It was observed that miR‑34a was upregulated in atherosclerotic plaque tissues and that ox‑LDL treatment significantly increased the levels of miR‑34a in a dose‑dependent manner in the HUVECs. The knockdown of miR‑34a increased the protein expression of B‑cell lymphoma 2 (Bcl‑2) and cell viability, improved mitochondrial membrane potential, and decreased the activity of caspase‑3, number of apoptotic cells and release of cytochrome c from mitochondria in the ox‑LDL‑treated HUVECs. The results also demonstrated that the knockdown of miR‑34a suppressed the levels of ox‑LDL‑induced reactive oxygen species (ROS) in HUVECs. Additionally, it was found that Bcl‑2 was a target of miR‑34a in HUVECs, and that silencing Bcl‑2 abrogated the protective effects of the downregulation of miR‑34a on ox‑LDL‑induced apoptosis. These data indicated that the knockdown of miR‑34a protected against ox‑LDL apoptosis and ROS in HUVECs via inhibiting the mitochondrial apoptotic pathway, suggesting it may offer potential as a biomarker in the clinical diagnosis and as a target for the treatment of atherosclerosis.

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Section: Knockdown Of Mir-34a Protects Against Ox-ldl-induced Rosmentioning

confidence: 87%

Section: Knockdown Of Mir-34a Prevents Ox-ldl-induced Huvec Apoptosismentioning

confidence: 99%

Downregulation of microRNA‑34a inhibits oxidized low‑density lipoprotein‑induced apoptosis and oxidative stress in human umbilical vein endothelial cells

Zhang

et al. 2018

Int J Mol Med

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“…However, there are other examples of miRNAs which are either downregulated (e.g., mir-29b, miR-200a/b) or upregulated (e.g., miR-155, mir-92a, miR-137) upon hyperglycemic/diabetic milieu in endothelial cells and contributing to endothelial inflammation and/or OxS deterioration. Specifically, these miRNAs were found to regulate redox balance via eNOS (miR-155), AMPKα1 (miR-137), O -GlcNAc transferase (OGT) (miR-200a/b) or components of Keap/Nrf2/HO-1 pathway (miR-92a, miR-200a) [ 245 , 246 , 247 , 248 , 249 , 250 ]. Interestingly, OxS was augmented due to lack of miR-29b-dependent regulation of AKT/eNOS signal pathway, as miR-29b was sponged by lncRNA H19 in vascular endothelium [ 245 ].…”

Section: Overview Of Mirnas—the Focus On Interplay With Oxidative mentioning

confidence: 99%

The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress

Włodarski

Strycharz

Wróblewski

et al. 2020

IJMS

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Oxidative stress (OxS) is the cause and the consequence of metabolic syndrome (MetS), the incidence and economic burden of which is increasing each year. OxS triggers the dysregulation of signaling pathways associated with metabolism and epigenetics, including microRNAs, which are biomarkers of metabolic disorders. In this review, we aimed to summarize the current knowledge regarding the interplay between microRNAs and OxS in MetS and its components. We searched PubMed and Google Scholar to summarize the most relevant studies. Collected data suggested that different sources of OxS (e.g., hyperglycemia, insulin resistance (IR), hyperlipidemia, obesity, proinflammatory cytokines) change the expression of numerous microRNAs in organs involved in the regulation of glucose and lipid metabolism and endothelium. Dysregulated microRNAs either directly or indirectly affect the expression and/or activity of molecules of antioxidative signaling pathways (SIRT1, FOXOs, Keap1/Nrf2) along with effector enzymes (e.g., GPx-1, SOD1/2, HO-1), ROS producers (e.g., NOX4/5), as well as genes of numerous signaling pathways connected with inflammation, insulin sensitivity, and lipid metabolism, thus promoting the progression of metabolic imbalance. MicroRNAs appear to be important epigenetic modifiers in managing the delicate redox balance, mediating either pro- or antioxidant biological impacts. Summarizing, microRNAs may be promising therapeutic targets in ameliorating the repercussions of OxS in MetS.

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“…As for the NF- κ B transcription factor, it is involved in many cell type challenges and pathogenic stimuli, including virus, bacterial, stress, and inflammatory cytokines. HIF-1 is a factor that is related to hypoxia, and ATF4 is an activating transcription factor that can upregulate some genes [12, 92, 93].…”

Section: Uv-related Signal Pathways and Transcription Involved In mentioning

confidence: 99%

Heme Oxygenases: Cellular Multifunctional and Protective Molecules against UV-Induced Oxidative Stress

Chen

Wang

Nisar

et al. 2019

Oxidative Medicine and Cellular Longevity

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Ultraviolet (UV) irradiation can be considered as a double-edged sword: not only is it a crucial environmental factor that can cause skin-related disorders but it can also be used for phototherapy of skin diseases. Inducible heme oxygenase-1 (HO-1) in response to a variety of stimuli, including UV exposure, is vital to maintain cell homeostasis. Heme oxygenase-2 (HO-2), another member of the heme oxygenase family, is constitutively expressed. In this review, we discuss how heme oxygenase (HO), a vital rate-limiting enzyme, participates in heme catabolism and cytoprotection. Phylogenetic analysis showed that there may exist a functional differentiation between HO-1 and HO-2 during evolution. Furthermore, depending on functions in immunomodulation and antioxidation, HO-1 participates in disease progression, especially in pathogenesis of skin diseases, such as vitiligo and psoriasis. To further investigate the particular role of HO-1 in diseases, we summarized the profile of the HO enzyme system and its related signaling pathways, such as Nrf2 and endoplasmic reticulum crucial signaling, both known to regulate HO-1 expression. Furthermore, we report on a C-terminal truncation of HO-1, which is generally considered as a signal molecule. Also, a newly identified alternative splice isoform of HO-1 not only provides us a novel perspective on comprehensive HO-1 alternative splicing but also offers us a basis to clarify the relationship between HO-1 transcripts and oxidative diseases. To conclude, the HO system is not only involved in heme catabolism but also involved in biological processes related to the pathogenesis of certain diseases, even though the mechanism of disease progression still remains sketchy. Further understanding the role of the HO system and its relationship to UV is helpful for revealing the HO-related signaling networks and the pathogenesis of many diseases.

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Downregulation of microRNA-155 ameliorates high glucose-induced endothelial injury by inhibiting NF-κB activation and promoting HO-1 and NO production

Cited by 9 publications

References 49 publications

Downregulation of microRNA‑34a inhibits oxidized low‑density lipoprotein‑induced apoptosis and oxidative stress in human umbilical vein endothelial cells

Downregulation of microRNA‑34a inhibits oxidized low‑density lipoprotein‑induced apoptosis and oxidative stress in human umbilical vein endothelial cells

The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress

Heme Oxygenases: Cellular Multifunctional and Protective Molecules against UV-Induced Oxidative Stress

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