Knock-Down of Long Non-Coding RNA ANRIL Suppresses Mouse Mesangial
                    Cell Proliferation, Fibrosis, Inflammation via Regulating
                    Wnt/β-Catenin and MEK/ERK Pathways in Diabetic
                    Nephropathy

Fang, Xun; Hu, Jun; Zhou, Haoming

doi:10.1055/a-1185-9283

Cited by 12 publications

(9 citation statements)

References 20 publications

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“…Cerebral ischemia and ischemia-reperfusion injury cause an inflammatory cascade reaction, including inflammatory cell infiltration, release of toxic inflammatory mediators and oxidative stress and excitotoxicity, thus leading to further nerve tissue damage and cell death (13). Over recent years, multiple studies have reported that anril regulates the inflammatory response and proliferation of cells through different signaling pathways in pathological aspects of ischemic stroke (14)(15)(16). For example, Zhao reported that lncRNA ANRIL knockdown improves cerebral infarction-induced neurological deficits and decreases the number of apoptotic neurons in an animal model.…”

Section: Introductionmentioning

confidence: 99%

ANRIL overexpression globally induces expression and alternative splicing of genes involved in inflammation in HUVECs

Alimu

Luohemanjiang

et al. 2022

Mol Med Rep

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long non-coding (lnc)rnas serve important cellular functions and certain lncrnas have roles in different mechanisms of gene regulation. lncrna-antisense non-coding rna in the INK4 locus (ANRIL) affects cell inflammation; however, the potential genes underlying the inflammatory response regulated by anril remain unclear. in the present study, the potential function of anril in regulating gene expression and alternative splicing was assessed. ANRIL-regulated human umbilical vein endothelial cell (HUVEC) transcriptome was obtained using high-throughput rna sequencing (rna-seq) to evaluate the potential role of ANRIL. Following plasmid transfection, gene expression profile and alternative splicing pattern of HUVECs overexpressing ANRIL were analyzed using rna-seq. anril overexpression affected the transcription levels of genes associated with the inflammatory response, nF-κB signaling pathway, type I interferon-mediated signal transduction pathway and innate immune response. ANRIL regulated the alternative splicing of hundreds of genes with functions such as gene expression, translation, dna repair, rna processing and participation in the nF-κB signaling pathway. Many of these genes serve a key role in the inflammatory response. ANRIL-regulated inflammatory response may be achieved by regulating alternate splicing and transcription. The present study broadened the understanding of anril-mediated gene regulation mechanisms and clarified the role of ANRIL in mediating inflammatory response mechanisms.

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Section: Introductionmentioning

confidence: 99%

ANRIL overexpression globally induces expression and alternative splicing of genes involved in inflammation in HUVECs

Alimu

Luohemanjiang

et al. 2022

Mol Med Rep

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“… 86 Similarly, lncRNA ANRIL knockdown can suppress mouse mesangial cell proliferation, inflammation and fibrosis via ERK pathways in a diabetic nephropathy model. 148 Akt also participates in inhibiting cell apoptosis and reducing eNOS expression via the ERK pathway in a bilateral common carotid occlusion model. 149 …”

Section: Significant Role Of Long Noncoding Rnas In Cerebral Ischemiamentioning

confidence: 98%

Emerging Role of LncRNAs in Ischemic Stroke—Novel Insights into the Regulation of Inflammation

Pan

Jiao

Wei

et al. 2021

JIR

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As a crucial kind of pervasive gene, long noncoding RNAs (lncRNAs) are abundant and key players in brain function as well as numerous neurological disorders, especially ischemic stroke. The mechanisms underlying ischemic stroke include angiogenesis, autophagy, apoptosis, cell death, and neuroinflammation. Inflammation plays a vital role in the pathological process of ischemic stroke, and systemic inflammation affects the patient's prognosis. Although a great deal of research has illustrated that various lncRNAs are closely relevant to regulate neuroinflammation and microglial activation in ischemic stroke, the specific interactional relationships and mechanisms between lncRNAs and neuroinflammation have not been described clearly. This review aimed to summarize the therapeutic effects and action mechanisms of lncRNAs on ischemia by regulating inflammation and microglial activation. In addition, we emphasize that lncRNAs have the potential to modulate inflammation by inhibiting and activating various signaling pathways, such as microRNAs, NF-κB and ERK.

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“…Monocyte chemotactic protein 1 (MCP-1) belongs to a small cytokine of the CC chemokine family, which has been identified as an important proinflammatory cytokine secreted by monocytes, macrophages, fibroblasts, vascular endothelial cells, B cells, and smooth muscle cells during an inflammatory response. Moreover, MCP-1 has specific chemotactic activation on monocytes/macrophages [8][9][10]. Accordingly, the present study investigated the prognostic value of the combined assay of IL-6, NF-κB, and MCP-1 in diabetic nephropathy to provide a reference for future clinical practice.…”

Section: Introductionmentioning

confidence: 98%

Prognostic Value of Serum Interleukin-6, NF-κB plus MCP-1 Assay in Patients with Diabetic Nephropathy

Jibao

et al. 2022

Disease Markers

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Objective. To assess the prognostic value of serum interleukin-6 (IL-6), nuclear factor-κB (NF-κB), and monocyte chemoattractant protein 1(MCP-1) assay in patients with diabetic nephropathy. Methods. From May 2019 to March 2020, 104 patients with diabetic nephropathy treated in our institution assessed for eligibility were recruited and assigned at a ratio of 1 : 1 to either the observation group ([urinary albumin excretion rate (UAER)] of 30 mg-300 mg/24 h) or the research group ([UAER] >300 mg/24 h). IL-6, MCP-1, renal function indices, and NF-κB levels were determined, and their correlation with DN was analyzed. Logistic regression was used to analyze the influencing factors of end-stage renal disease in patients with diabetic nephropathy. The receiver operating characteristic (ROC) curve was drawn, and the area under the curve (AUC) was calculated to analyze the predictive value of combined detection of IL-6, MCP-1, and NF-κB in the prognosis of patients with diabetic nephropathy. Results. The eligible patients with UAER of 30 mg-300 mg/24 h were associated with significantly higher levels of IL-6, MCP-1, NF-κB, blood urea nitrogen (BUN), and serum creatinine (Scr) versus those with UAER >300 mg/24 h ( P < 0.05 ). During the follow-up, a total of 38 patients progressed to end-stage renal diseases. Eligible patients with end-stage renal diseases showed significantly higher serum IL-6, MCP-1, and NF-κB levels versus those without end-stage renal diseases ( P < 0.05 ). Serum IL-6, MCP-1, and NF-κB are independent risk factors for the occurrence of end-stage renal disease in patients with diabetic nephropathy. The AUCs of IL-6, MCP-1, and NF-κB for predicting the prognosis of patients with diabetic nephropathy were 0.562, 0.634, and 0.647, respectively, and the AUC of the three combined detection for predicting the prognosis of patients with diabetic nephropathy was 0.889. Conclusion. Serum IL-6, NF-κB, and MCP-1 levels are closely related to renal injury and poor prognosis in patients with diabetic nephropathy, and the combined assay is valuable for assessing patients’ condition and prognosis.

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Knock-Down of Long Non-Coding RNA ANRIL Suppresses Mouse Mesangial Cell Proliferation, Fibrosis, Inflammation via Regulating Wnt/β-Catenin and MEK/ERK Pathways in Diabetic Nephropathy

Cited by 12 publications

References 20 publications

ANRIL overexpression globally induces expression and alternative splicing of genes involved in inflammation in HUVECs

ANRIL overexpression globally induces expression and alternative splicing of genes involved in inflammation in HUVECs

Emerging Role of LncRNAs in Ischemic Stroke—Novel Insights into the Regulation of Inflammation

Prognostic Value of Serum Interleukin-6, NF-κB plus MCP-1 Assay in Patients with Diabetic Nephropathy

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