scholarly journals miR-181c-5p Exacerbates Hypoxia/Reoxygenation-Induced Cardiomyocyte Apoptosis via Targeting PTPN4

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Liang Ge ◽  
Yin Cai ◽  
Fan Ying ◽  
Hao Liu ◽  
Dengwen Zhang ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Control Cell ◽  
Luciferase Reporter ◽  
Apoptosis Pathway ◽  
H9c2 Cardiomyocytes ◽  
Hypoxia Reoxygenation

Background. Activation of cell apoptosis is a major form of cell death during myocardial ischemia/reperfusion injury (I/RI). Therefore, examining ways to control cell apoptosis has important clinical significance for improving postischemic recovery. Clinical evidence demonstrated that miR-181c-5p was significantly upregulated in the early phase of myocardial infarction. However, whether or not miR-181c-5p mediates cardiac I/RI through cell apoptosis pathway is unknown. Thus, the present study is aimed at investigating the role and the possible mechanism of miR-181c-5p in apoptosis during I/R injury by using H9C2 cardiomyocytes. Methods and Results. The rat origin H9C2 cardiomyocytes were subjected to hypoxia/reoxygenation (H/R, 6 hours hypoxia followed by 6 hours reoxygenation) to induce cell injury. The results showed that H/R significantly increased the expression of miR-181c-5p but not miR-181c-3p in H9C2 cells. In line with this, in an in vivo rat cardiac I/RI model, miR-181c-5p expression was also significantly increased. The overexpression of miR-181c-5p by its agomir transfection significantly aggravated H/R-induced cell injury (increased lactate dehydrogenase level and reduced cell viability) and exacerbated H/R-induced cell apoptosis (greater cleaved caspases 3 expression, Bax/Bcl-2 and more TUNEL-positive cells). In contrast, inhibition of miR-181c-5p in vitro had the opposite effect. By using computational prediction algorithms, protein tyrosine phosphatase nonreceptor type 4 (PTPN4) was predicted as a potential target gene of miR-181c-5p and was verified by the luciferase reporter assay. The overexpression of miR-181c-5p significantly attenuated the mRNA and protein expression of PTPN4 in H9C2 cardiomyocytes. Moreover, knockdown of PTPN4 significantly aggravated H/R-induced enhancement of LDH level, cleaved caspase 3 expression, and apoptotic cell death, which mimicked the proapoptotic effects of miR-181c-5p in H9C2 cardiomyocytes. Conclusions. These findings suggested that miR-181c-5p exacerbates H/R-induced cardiomyocyte injury and apoptosis via targeting PTPN4 and that miR-181c-5p/PTPN4 signaling may yield novel strategies to combat myocardial I/R injury.

Abstract 319: Mirna-125b Reduces Ischemia / Reperfusion (i/r)-induced Apoptosis Through Targeting Multiple Targets in Intrinsic and Extrinsic Apoptosis Pathways

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Peipei Wang ◽  
Qiying Chen ◽  
Yue Zhou ◽  
Arthur M Richards
Keyword(s):  
Cell Count ◽  
Cell Injury ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Neonatal Rat ◽  
Luciferase Reporter ◽  
Protective Effects ◽  
Extrinsic Pathway ◽  
Multiple Genes ◽  
Induced Apoptosis

Apoptosis is mediated through extrinsic and intrinsic pathways, both play a role in ischemia/reperfusion (I/R) injury. Predicted targets for miRNA-125b include extrinsic pathway mediators Traf6 and Tnfrsf1b, and intrinsic mitochondria regulators Bcl-2 family pro-apoptotic effectors Bak1 and BH3-only facilitators Bim, Bmf, Puma. We hypothesized that miRNA-125b directly targets multiple genes to reduce I/R-induced apoptosis. Myoblast H9c2 cells underwent 16 hours 0.2% O 2 hypoxia followed by 2 hours re-oxygenation (H-R, simulating I/R) and were transfected with miRNA-125b mimic vs. scrambled mimic control (25 nmol, miR-125b-M vs. MC) and miR-125b inhibitor vs. inhibitor control (miR-125b-I vs. IC). Cell count/viability, WST assay, cell injury-induced LDH release and apoptotic marker Casp3/7 were measured. Cells were trypsinized for assessment of apoptosis (7-AAD and annexin V double staining) and lysed for RT-qPCR and western blot (WB) analyses. pCMV-Myc-Bak1 plasmids were cloned and transfected into H9c2 for recovery studies. The effects were verified in neonatal rat ventricular myocytes (NRVM). miRNA-125b-M significantly reduced H-R injury as indicated by higher cell count/viability and WST activity, and reduced LDH (miR-125b-M vs. MC p<0.05). qPCR confirmed that (1) miR-125b expression was reduced in H-R; (2) RISC-loaded (immunoprecipitation pull-down Ago-2) miR-125b increased by ~35 fold and reduced to ~3% following mimic and inhibitor transfection respectively; (3) multiple apoptosis-related genes were reduced by miR-125b-M, Bak1, Bmf, Bim, Puma, Traf6 and Tnfrsf1b. All changes were confirmed by WB. Luciferase reporter assays indicated miR-125b bound to the 3’-UTR of all genes tested except Traf6. Total apoptotic cell numbers and Casp3/7 release were significantly reduced by miR-125b-M. The protective effect of miRNA-125b was partially abolished by Bak1 overexpression (pCMV-Myc-Bak1 and miR-125b co-transfection). Protective effects of miRNA-125b were further verified in NRVM. MiRNA-125b inhibitor reversed protective effects and target changes at mRNA and protein level. miR-125b is powerfully cardioprotective in I/R injury due to directly targeting multiple genes in the extrinsic and intrinsic apoptotic pathways.

Abstract 100: A Novel Anti-cell Death Mechanism by Targeting the Biosynthesis of Oligosaccharide in ER

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Xiangwei Luo ◽  
Wenjuan Zhou ◽  
Lingling Wei ◽  
Liang Wei ◽  
Fengxue Zhang
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Hsp90 Inhibitor ◽  
Parp Cleavage ◽  
Apoptosis Pathway ◽  
Cell Death Pathway ◽  
Multiple Cell ◽  
The Unfolded Protein Response

The pathological expression of many of the deadly human diseases such as myocardial infarction, renal failure etc. is cell death. In cancer research, myriads of ways have been found to kill a cell. However, we are still craving for an applicable mechanism to prevent cell death. The majority of the current research is to directly target the apoptosis pathway. While some compounds have been developed, none of them are pharmaceutically important likely due to the inherent toxic nature of the target. Here, we report a novel mechanism to block the cell death pathway by activating the cells’ own protective programs coded for stress. Components of the unfolded protein response (UPS) in ER have been implicated in the protection of ischemia/reperfusion heart in recent research. By targeting the biosynthesis of oligosaccharide, which activated UPS as indicated by the expression of the ER chaperones Grp94 and Grp78, we were able to completely block the Hsp90 inhibitor induced apoptotic cell death as well as the oxidative stress (as exemplified by sodium nitroprusside, SNP) induced necrotic cell death in multiple cell lines. Caspase-3 activation and PARP cleavage were nearly completely inhibited. While awaiting further exploration, the biosynthesis of the oligosaccharide could turn out to be an applicable target for acute conditions such as cardiac injury because of its relatively safe nature.

scholarly journals Upregulation of microRNA-876 Induces Endothelial Cell Apoptosis by Suppressing Bcl-Xl in Development of Atherosclerosis

2017 ◽  
Vol 42 (4) ◽  
pp. 1540-1549 ◽  
Author(s):  
Kaicheng Xu ◽  
Peng Liu ◽  
Yue Zhao
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Endothelial Cell ◽  
Aortic Arch ◽  
Cell Apoptosis ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Luciferase Reporter ◽  
Endothelial Cell Apoptosis

Background/Aims: The injury and apoptotic cell death of endothelial cells hallmark the development of atherosclerosis (AS), characterized by dysregulation of lipid homeostasis, immune responses, and formation of coronary plaques. However, the mechanisms underlying the initiation of endothelial cell apoptosis remain ill-defined. Recent evidence suggests a role of microRNAs in the processes of AS-associated endothelial cell apoptosis. Thus, we studied this question in the current study. Methods: AS was developed in ApoE (-/-) mice suppled with high-fat diet (HFD), compared to ApoE (-/-) mice suppled with normal diet (ND). Mouse endothelial cells were isolated from the aortic arch using flow cytometry based on their expression of Pecam-1. Oxidized low-density lipoprotein (ox-LDL) were used to treat human aortic endothelial cells (HAECs) as an in vitro model for AS. Gene expression was quantified by RT-qPCR and protein levels were analyzed by Western blotting. Apoptosis was evaluated by FITC Annexin V Apoptosis essay and by TUNEL staining. Prediction of the binding between miRNAs and 3'-UTR of mRNA from the target gene was performed by bioinformatics analyses and confirmed by a dual luciferase reporter assay. Results: HFD mice, but not ND mice, developed AS in 12 weeks. Significantly reduced endothelial cell marks and significantly increased mesenchymal cell marks were detected in the aortic arch of the HFD mice, compared to the ND mice. The endothelial cell apoptosis was significantly higher in HFD mice, seemingly due to functional suppression of protein translation of anti-apoptotic Bcl-Xl protein through upregulation of miR-876. Similar results were obtained from in vitro study. Inhibition of miR-876 abolished the effects of ox-LDL-induced apoptotic cell death of HAECs. Conclusion: AS-associated endothelial cell apoptosis may partially result from downregulation of Bcl-Xl, through upregulation of miR-876 that binds and suppresses translation of Bcl-Xl mRNA.

scholarly journals MicroRNA‐181c‐5p exacerbates apoptotic cell death in H9C2 cardiomyocytes during hypoxia/reoxygenation

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Liang Ge ◽  
Haichun Ma ◽  
Yin Cai ◽  
Lei Pang ◽  
Michael G. Irwin ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
H9c2 Cardiomyocytes ◽  
Hypoxia Reoxygenation

scholarly journals miR-210 Regulates Apoptotic Cell Death during Cellular Hypoxia and Reoxygenation in a Diametrically Opposite Manner

Biomedicines ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 42
Author(s):  
Gurdeep Marwarha ◽  
Øystein Røsand ◽  
Nathan Scrimgeour ◽  
Katrine Hordnes Slagsvold ◽  
Morten Andre Høydal
Keyword(s):  
Cell Death ◽  
Cellular Response ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Biological Response ◽  
Apoptotic Cell Death ◽  
Cellular Mechanisms ◽  
Apoptosis Pathway ◽  
Intrinsic Apoptosis Pathway ◽  
Opposite Manner

Apoptotic cell death of cardiomyocytes is a characteristic hallmark of ischemia–reperfusion (I/R) injury. The master hypoxamiR, microRNA-210 (miR-210), is considered the primary driver of the cellular response to hypoxic stress. However, to date, no consensus has emerged with regards to the polarity of the miR-210-elicited cellular response, as miR-210 has been shown to exacerbate as well as attenuate hypoxia-driven apoptotic cell death. Herein, in AC-16 cardiomyocytes subjected to hypoxia-reoxygenation (H-R) stress, we unravel novel facets of miR-210 biology and resolve the biological response mediated by miR-210 into the hypoxia and reoxygenation temporal components. Using transient overexpression and decoy/inhibition vectors to modulate miR-210 expression, we elucidated a Janus role miR-210 in the cellular response to H-R stress, wherein miR-210 mitigated the hypoxia-induced apoptotic cell death but exacerbated apoptotic cell death during cellular reoxygenation. We further delineated the underlying cellular mechanisms that confer this diametrically opposite effect of miR-210 on apoptotic cell death. Our exhaustive biochemical assays cogently demonstrate that miR-210 attenuates the hypoxia-driven intrinsic apoptosis pathway, while significantly augmenting the reoxygenation-induced caspase-8-mediated extrinsic apoptosis pathway. Our study is the first to unveil this Janus role of miR-210 and to substantiate the cellular mechanisms that underlie this functional duality.

scholarly journals MiR-181c-5p Promotes Inflammatory Response during Hypoxia/Reoxygenation Injury by Downregulating Protein Tyrosine Phosphatase Nonreceptor Type 4 in H9C2 Cardiomyocytes

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Sheng Wang ◽  
Liang Ge ◽  
Dengwen Zhang ◽  
Lin Wang ◽  
Hao Liu ◽  
...  
Keyword(s):  
Proinflammatory Cytokines ◽  
Protein Tyrosine Phosphatase ◽  
Cell Injury ◽  
Ischemia Reperfusion ◽  
Tyrosine Phosphatase ◽  
Protein Tyrosine ◽  
H9c2 Cardiomyocytes ◽  
Hypoxia Reoxygenation

Background. Constitutive nuclear factor kappa B (NFκB) activation has been shown to exacerbate during myocardial ischemia/reperfusion (I/R) injury. We recently showed that miR-181c-5p exacerbated cardiomyocytes injury and apoptosis by directly targeting the 3′-untranslated region of protein tyrosine phosphatase nonreceptor type 4 (PTPN4). However, whether miR-181c-5p mediates cardiac I/R injury through NFκB-mediated inflammation is unknown. Thus, the present study aimed to investigate the role of miR-181c-5p during myocardial I/R injury and explore its mechanism in relation to inflammation in H9C2 cardiomyocytes. Methods and Results. In hypoxia/reoxygenation (H/R, 6 h hypoxia followed by 6 h reoxygenation)-stimulated H9C2 cardiomyocytes or postischemic myocardium of rat, the expression of miR-181c-5p was significantly upregulated, which was concomitant increased NFκB activity when compared to the nonhypoxic or nonischemic control groups. This is indicative that miR-181c-5p may be involved in NFκB-mediated inflammation during myocardial I/R injury. To investigate the potential role of miR-181c-5p in H/R-induced cell inflammation and injury, H9C2 cardiomyocytes were transfected with the miR-181c-5p agomir. Overexpression of miR-181c-5p significantly aggravated H/R-induced cell injury (increased lactate dehydrogenase (LDH) level) and exacerbated NFκB-mediated inflammation (greater phosphorylation and degradation of IκBα, phosphorylation of p65, and increased levels of proinflammatory cytokines tumor necrosis factor α (TNFα), interleukin (IL)-6, and IL-1β). In contrast, inhibition of miR-181c-5p by its antagomir transfection in vitro had the opposite effect. Furthermore, overexpression of miR-181c-5p significantly enhanced lipopolysaccharide-induced NFκB signalling. Additionally, knockdown of PTPN4, the direct target of miR-181c-5p, significantly aggravated H/R-induced phosphorylation and degradation of IκBα, phosphorylation of p65, and the levels of proinflammatory cytokines. PTPN4 knockdown also cancelled miR-181c-5p antagomir mediated anti-inflammatory effects in H9C2 cardiomyocytes during H/R injury. Conclusions. It is concluded that miR-181c-5p may exacerbate myocardial I/R injury and NFκB-mediated inflammation via PTPN4, and that targeting miR-181c-5p/PTPN4/NFκB signalling may represent a novel strategy to combat myocardial I/R injury.

scholarly journals Cox-2 Inhibition Protects against Hypoxia/Reoxygenation-Induced Cardiomyocyte ApoptosisviaAkt-Dependent Enhancement of iNOS Expression

2016 ◽  
Vol 2016 ◽  
pp. 1-17 ◽  
Author(s):  
Lei Pang ◽  
Yin Cai ◽  
Eva Hoi Ching Tang ◽  
Dan Yan ◽  
Ramoji Kosuru ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Injury ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Specific Inhibitor ◽  
Protective Effects ◽  
Rat Cardiomyocytes ◽  
Phosphorylated Akt ◽  
Cox 2 ◽  
Hypoxia Reoxygenation

The present study explored the potential causal link between ischemia-driven cyclooxygenase-2 (COX-2) expression and enhanced apoptosis during myocardial ischemia/reperfusion (I/R) by using H9C2 cardiomyocytes and primary rat cardiomyocytes subjected to hypoxia/reoxygenation (H/R). The results showed that H/R resulted in higher COX-2 expression than that of controls, which was prevented by pretreatment with Helenalin (NFκB specific inhibitor). Furthermore, pretreatment with NS398 (COX-2 specific inhibitor) significantly attenuated H/R-induced cell injury [lower lactate dehydrogenase (LDH) leakage and enhanced cell viability] and apoptosis (higher Bcl2 expression and lower level of cleaved caspases-3 and TUNEL-positive cells) in cardiomyocytes. The amelioration of posthypoxic apoptotic cell death was paralleled by significant attenuation of H/R-induced increases in proinflammatory cytokines [interleukin 6 (IL6) and tumor necrosis factor (TNFα)] and reactive oxygen species (ROS) production and by higher protein expression of phosphorylated Akt and inducible nitric oxide synthase (iNOS) and enhanced nitric oxide production. Moreover, the application of LY294002 (Akt-specific inhibitor) or 1400W (iNOS-selective inhibitor) cancelled the cellular protective effects of NS398. Findings from the current study suggest that activation of NFκB during cardiomyocyte H/R induces the expression of COX-2 and that higher COX-2 expression during H/R exacerbates cardiomyocyte H/R injuryviamechanisms that involve cross talks among inflammation, ROS, and Akt/iNOS/NO signaling.

Quercetin in attenuation of ischemic/reperfusion injury: A review

2020 ◽  
Vol 13 ◽  
Author(s):  
Milad Ashrafizadeh ◽  
Saeed Samarghandian ◽  
Kiavash Hushmandi ◽  
Amirhossein Zabolian ◽  
Md Shahinozzaman ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Membrane ◽  
Blood Supply ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Membrane Integrity ◽  
Therapeutic Effects ◽  
Molecular Pathways ◽  
Cell Membrane Integrity ◽  
Cell Membrane Disruption

Background: Ischemia/reperfusion (I/R) injury is a serious pathologic event that occurs due to restriction in blood supply to an organ, followed by hypoxia. This condition leads to enhanced levels of pro-inflammatory cytokines such as IL-6 and TNF-, and stimulation of oxidative stress via enhancing reactive oxygen species (ROS) levels. Upon reperfusion, blood supply increases, but it deteriorates condition, and leads to generation of ROS, cell membrane disruption and finally, cell death. Plant derived-natural compounds are well-known due to their excellent antioxidant and anti-inflammatory activities. Quercetin is a flavonoid exclusively found in different vegetables, herbs, and fruits. This naturally occurring compound possesses different pharmacological activities making it appropriate option in disease therapy. Quercetin can also demonstrate therapeutic effects via affecting molecular pathways such as NF-B, PI3K/Akt and so on. Methods: In the present review, we demonstrate that quercetin administration is beneficial in ameliorating I/R injury via reducing ROS levels, inhibition of inflammation, and affecting molecular pathways such as TLR4/NF-B, MAPK and so on. Results and conclusion: Quercetin can improve cell membrane integrity via decreasing lipid peroxidation. Apoptotic cell death is inhibited by quercetin via down-regulation of Bax, and caspases, and upregulation of Bcl-2. Quercetin is able to modulate autophagy (inhibition/induction) in decreasing I/R injury. Nanoparticles have been applied for delivery of quercetin, enhancing its bioavailability and efficacy in alleviation of I/R injury. Noteworthy, clinical trials have also confirmed the capability of quercetin in reducing I/R injury.

scholarly journals CircHIPK3 regulates the autophagy and apoptosis of hypoxia/reoxygenation-stimulated cardiomyocytes via the miR-20b-5p/ATG7 axis

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Zhimei Qiu ◽  
Yan Wang ◽  
Weiwei Liu ◽  
Chaofu Li ◽  
Ranzun Zhao ◽  
...  
Keyword(s):  
Cell Injury ◽  
Ischemia Reperfusion ◽  
Circular Rna ◽  
Control Group ◽  
Loss Of Function ◽  
Cardiomyocyte Autophagy ◽  
Myocardial Ischemia Reperfusion ◽  
Injury Research ◽  
Hypoxia Reoxygenation

AbstractAutophagy and apoptosis are involved in myocardial ischemia/reperfusion (I/R) injury. Research indicates that circular RNA HIPK3 (circHIPK3) is crucial to cell autophagy and apoptosis in various cancer types. However, the role of circHIPK3 in the regulation of cardiomyocyte autophagy and apoptosis during I/R remains unknown. Our study aimed to examine the regulatory effect of circHIPK3 during myocardial I/R and investigate its mechanism in cardiomyocyte autophagy and apoptosis. Methods and results. The expression of circHIPK3 was upregulated during myocardial I/R injury and hypoxia/reoxygenation (H/R) injury of cardiomyocytes. To study the potential role of circHIPK3 in myocardial H/R injury, we performed gain-of-function and loss-of-function analyses of circHIPK3 in cardiomyocytes. Overexpression of circHIPK3 significantly promoted H/R-induced cardiomyocyte autophagy and cell injury (increased intracellular reactive oxygen species (ROS) and apoptosis) compared to those in the control group, while silencing of circHIPK3 showed the opposite effect. Further research found that circHIPK3 acted as an endogenous miR-20b-5p sponge to sequester and inhibit miR-20b-5p activity, resulting in increased ATG7 expression. In addition, miR-20b-5p inhibitors reversed the decrease in ATG7 induced by silencing circHIPK3. Conclusions. CircHIPK3 can accelerate cardiomyocyte autophagy and apoptosis during myocardial I/R injury through the miR-20b-5p/ATG7 axis. These data suggest that circHIPK3 may serve as a potential therapeutic target for I/R.

scholarly journals NEAT1 aggravates sepsis-induced acute kidney injury by sponging miR-22-3p

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 333-342
Author(s):  
Yawei Feng ◽  
Jun Liu ◽  
Ranliang Wu ◽  
Peng Yang ◽  
Zhiqiang Ye ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Western Blot ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Cell Injury ◽  
Kidney Injury ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Western Blot Assay

AbstractBackground and aimAcute kidney injury (AKI) is a common complication of sepsis. Long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) plays a vital role in various diseases, including AKI. This study aimed to investigate the function and mechanism of NEAT1 in sepsis-induced AKI.Materials and methodsA septic AKI model was established by treating HK-2 cells with lipopolysaccharide (LPS). The levels of NEAT1 and miR-22-3p were measured by quantitative real-time PCR. Cell apoptosis was assessed by flow cytometry. The levels of apoptosis-related protein and autophagy-related factors were examined by the western blot assay. An enzyme-linked immunosorbent assay was used to calculate the contents of inflammatory factors. The interaction between NEAT1 and miR-22-3p was validated by dual-luciferase reporter assay, RNA immunoprecipitation assay, and RNA pull-down assay. The levels of nuclear factor (NF)-κB pathway-related proteins were evaluated by the western blot assay.ResultsNEAT1 was upregulated, while miR-22-3p was downregulated in patients with sepsis and in LPS-stimulated HK-2 cells. LPS treatment triggered cell apoptosis, autophagy, and inflammatory response in HK-2 cells. NEAT1 knockdown attenuated LPS-induced cell injury. NEAT1 modulated LPS-triggered cell injury by targeting miR-22-3p. Furthermore, NEAT1 regulated the NF-κB pathway by modulating miR-22-3p.ConclusionDepletion of NEAT1 alleviated sepsis-induced AKI via regulating the miR-22-3p/NF-κB pathway.

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