LncRNA TapSAKI promotes inflammation injury in HK-2 cells and urine derived sepsis-induced kidney injury

Shen, Jun; Liu, Li; Zhang, Facai; Gu, Jiang; Pan, Guanghui

doi:10.1111/jphp.13049

Cited by 56 publications

(37 citation statements)

References 26 publications

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“…in other words, silencing of Hulc ameliorated the lPS-mediated injury in HMec-1 cells, which was consistent with a previous report (9). Multiple reports have proposed that lncrnas play pivotal roles in sepsis by targeting miRNAs (6,7). For example, NEAT1 upregulated Toll-like receptor 4 to promote sepsis-induced liver injury by sponging let-7a (29).…”

Section: Discussionsupporting

confidence: 90%

“…lncrnas have roles in the regulation of inflammatory responses in sepsis (5). For example, lncrna Transcript Predicting Survival in aKi was demonstrated to facilitate HK-2 cell apoptosis and inflammatory responses in sepsis-induced kidney injury (6). lncRNA hox transcript antisense rna could repress proliferation, and upregulate apoptosis and inflammatory responses in sepsis in vitro (7).…”

Section: Introductionmentioning

confidence: 99%

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Potential role of lncRNA HULC/miR‑128‑3p/RAC1 axis in the inflammatory response during LPS‑induced sepsis in HMEC‑1 cells

et al. 2020

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Sepsis is a serious clinical condition characterized by systemic inflammation. The long noncoding rna (lncrna) highly upregulated in liver cancer (Hulc) was validated to partake in the development of sepsis. The present study aimed to investigate the potential mechanism of Hulc in lipopolysaccharide (lPS)-induced sepsis. reverse transcription-quantitative polymerase chain reaction (rT-qPcr) and western blot analysis was employed to examine the expression of Hulc, microrna (mir)-128-3p, rac family small GTPase 1 (RAC1) and pro-inflammatory factors [IL-6, TnF-α, intercellular adhesion molecule (icaM1) and vascular cell adhesion molecule (VcaM1)] in the serum of patients with sepsis or lPS-induced human dermal microvascular endothelial cells (HMec-1). Flow cytometry and western blot assays were performed to detect cell apoptosis. The targeted relationship among HULC, miR-128-3p and RAC1 was confirmed by a dual-luciferase reporter assay, rna binding protein immunoprecipitation (riP) assay and rna pull-down assay. Hulc and rac1 were found to be upregulated, and mir-128-3p was downregulated in the serum of patients with sepsis and lPS-stimulated HMec-1 cells. lPS promoted apoptosis and inflammation, which were decreased by silencing of HULC. Hulc targeted mir-128-3p and negatively regulated its expression. Hulc knockdown protected HMec-1 cells from lPS-induced injury by upregulating mir-128-3p. rac1 was a target of mir-128-3p, and gain of rac1 also relieved the silencing of Hulc-mediated suppressive effects on apoptosis and inflammation in LPS-stimulated HMEC-1 cells. In conclusion, Hulc knockdown partially reversed lPS-induced sepsis via the regulation of mir-128-3p/rac1 axis.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Potential role of lncRNA HULC/miR‑128‑3p/RAC1 axis in the inflammatory response during LPS‑induced sepsis in HMEC‑1 cells

et al. 2020

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“…TLR4, an important regulator of the NF-κB signaling pathway, has been shown to regulate cell apoptosis, inflammatory response and oxidative damage of renal tubular epithelial cell in hyperglycemia [42,43]. Notably, a previous study showed that miR-140-5p inhibits pulmonary inflammatory response in ALI by targeting TLR4 [18].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-140-5p ameliorates the high glucose-induced apoptosis and inflammation through suppressing TLR4/NF-κB signaling pathway in human renal tubular epithelial cells

Ren

Chen

et al. 2020

Bioscience Reports

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Hyperglycemia-induced renal tubular cell injury is thought to play a critical role in the pathogenesis of diabetic nephropathy (DN). However, the role of miRNAs in renal tubular cell injury remains to be fully elucidated. The aim of the present study was to investigate the role and mechanisms of miRNAs protecting against high glucose (HG)-induced apoptosis and inflammation in renal tubular cells. First, we analyzed microRNA (miRNA) expression profiles in kidney tissues from DN patients using miRNA microarray. It was observed that miRNA-140-5p (miR-140-5p) was significantly down-regulated in kidney tissues from patients with DN. An inverse correlation between miR-140-5p expression levels with serum proteinuria was observed in DN patients, suggesting miR-140-5p may be involved in the progression of DN. HG-induced injury in HK-2 cells was used to explore the potential role of miR-140-5p in DN. We found that miR-140-5p overexpression improved HG-induced cell injury, as evidenced by the enhancement of cell viability, and inhibition of the activity of caspase-3 and reactive oxygen species (ROS) generation. It was also observed that up-regulation of miR-140-5p suppressed HG induced the expressions of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 in HK-2 cells. In addition, TLR4, one of the upstream molecules of NF-κB signaling pathway, was found to be a direct target of miR-140-5p in the HK-2. Moreover, the HG-induced activation of NF-κB signaling pathway was inhibited by miR-140-5p overexpression. These results indicated that miR-140-5p protected HK-2 cells against HG-induced injury through blocking the TLR4/NF-κB pathway, and miR-140-5p may be considered as a potential prognostic biomarker and therapeutic target in the treatment of DN.

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“…LncRNA can regulate inflammatory response via regulating the related proteins. For example, TapSAKI aggravates inflammatory injury of HK‐2 cells and renal insufficiency induced by urogenic sepsis; upregulation of circulating NEAT1 is closely linked to increased severity and adverse prognosis of sepsis patients . Some studies highlight the significance of CRNDE in diverse diseases.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA colorectal neoplasia differentially expressed alleviates sepsis‐induced liver injury via regulating miR‐126‐5p

Song²,

Xie

et al. 2020

IUBMB Life

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In this study, we intended to determine the detailed function and mechanism of long noncoding RNA (lncRNA) colorectal neoplasia differentially expressed (CRNDE) in liver injury induced by sepsis. Cecal ligation and perforation (CLP) models were adopted to induce sepsis in vivo with rats, and hepatic epithelial cells L02 were treated with lipopolysaccharide (LPS) to mimic sepsis in vitro. Enzyme‐linked immunosorbent assay was conducted to detect the levels of tumor necrosis factor (TNF‐α), interleukin‐6 (IL‐6), interleukin‐10 (IL‐10), and interferon‐γ (IFN‐γ) in the serum of rats. Quantitative real‐time polymerase chain reaction (qRT‐PCR) was performed to measure the expressions of CRNDE and microRNA‐126‐5p (miR‐126‐5p). Flow cytometry analysis and Cell Counting Kit‐8 (CCK‐8) method were carried out followed by the up‐ or downregulation of CRNDE and miR‐126‐5p to monitor the proliferation and apoptosis of L02 cells, respectively. Western blot was then applied to determine the expressions of cysteinyl aspartate specific proteinase 3 (caspase 3), poly(ADP‐ribose)polymerase (PARP), cytochrome c, and BCL2‐like 2 (BCL2L2). The interactions between CRNDE with miR‐126‐5p and miR‐126‐5p with BCL2L2 were determined through bioinformatics, qRT‐PCR, dual luciferase reporter assay, and RNA immunoprecipitation assay. CRNDE was significantly decreased in liver tissues and hepatic cells in sepsis models. Upregulation of CRNDE promoted the viability of L02 cells and inhibited their apoptosis, while downregulation of CRNDE had opposite effects. The expression of CRNDE in liver tissues of septic rats was correlated with the expression miR‐126‐5p. It was also demonstrated that the transfection of miR‐126‐5p mimics reversed the inhibitory effect induced by CRNDE on apoptosis of L02 cells. CRNDE could specifically bind to miR‐126‐5p and reduce its expression, in turn promote the expression of BCL2L2. Additionally, CRNDE overexpression in rats ameliorated liver injury induced by sepsis. Downregulated CRNDE aggravates hepatic injury via regulating miR‐126‐5p and BCL2L2 during sepsis.

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LncRNA TapSAKI promotes inflammation injury in HK-2 cells and urine derived sepsis-induced kidney injury

Cited by 56 publications

References 26 publications

Potential role of lncRNA HULC/miR‑128‑3p/RAC1 axis in the inflammatory response during LPS‑induced sepsis in HMEC‑1 cells

Potential role of lncRNA HULC/miR‑128‑3p/RAC1 axis in the inflammatory response during LPS‑induced sepsis in HMEC‑1 cells

MicroRNA-140-5p ameliorates the high glucose-induced apoptosis and inflammation through suppressing TLR4/NF-κB signaling pathway in human renal tubular epithelial cells

Long noncoding RNA colorectal neoplasia differentially expressed alleviates sepsis‐induced liver injury via regulating miR‐126‐5p

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