Effects of Long Non-Coding RNA LINC00963 on Renal Interstitial Fibrosis and Oxidative Stress of Rats with Chronic Renal Failure via the Foxo Signaling Pathway

Chen, Wen; Zhang, Lei; Zhou, Zhengyuan; Ren, Yueqin; Sun, Lina; Man, Yan-Gao; Ma, Zhilei; Wang, Zhikui

doi:10.1159/000488739

Cited by 50 publications

(32 citation statements)

References 40 publications

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“…Differentially expressed lnRNAs are determined in MI and co‐expressed with differentially expressed mRNAs, and their interactions are implicated in pathogenesis mechanism of MI . Silencing of ATP2B1‐AS1 can suppress renal interstitial fibrosis and oxidative stress in chronic renal failure . In this study, mouse ATP2B1‐AS1 silencing was suggested to inhibit the cardiomyocyte apoptosis and inflammation, suggesting a potential of ATP2B1‐AS1 in protection against MI.…”

Section: Discussionmentioning

confidence: 63%

“…Long non‐coding RNAs (lncRNAs) constitute a group of non‐coding RNAs implicated in diverse biological processes through regulation of gene expression and have recently been reported to be novel predictors in the setting of AMI . ATPase plasma membrane Ca 2+ transporting 1 antisense RNA 1 (ATP2B1‐AS1), also named long intergenic non‐protein‐coding RNA 936 (LINC00936), has been found to be an important regulator in chronic renal failure‐induced renal interstitial fibrosis and oxidative stress . However, the relationship between this lncRNA and MI remains to be defined.…”

Section: Introductionmentioning

confidence: 99%

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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: Discussionmentioning

confidence: 63%

Section: Introductionmentioning

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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“…Chen et al [68] reported that LINC00963 was highly expressed in CRF rats, and FoxO3 was verified as a target gene of LINC00963. Lower LINC00963 expression attenuated interstitial fibrosis and oxidative stress in chronic renal failure (CRF) by activation of the FoxO signaling pathway, which helps us to understand the potential gene mechanisms of CRF, and may provide new prognostic markers for 8 of 14 CRF treatment in the future.…”

Section: Linc00936mentioning

confidence: 99%

“…Lower LINC00963 expression attenuated interstitial fibrosis and oxidative stress in chronic renal failure (CRF) by activation of the FoxO signaling pathway, which helps us to understand the potential gene mechanisms of CRF, and may provide new prognostic markers for 8 of 14 CRF treatment in the future. However, they did not thoroughly investigate how LINC00963 affects the activation of the FoxO signaling pathway and the potential mechanism in interstitial fibrosis CRF [68].…”

Section: Linc00936mentioning

confidence: 99%

Potential Roles of Long Noncoding RNAs as Therapeutic Targets in Renal Fibrosis

Jung

Kim

Park

2020

IJMS

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Many studies have made clear that most of the genome is transcribed into noncoding RNAs, including microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), both of which can affect different cell features. LncRNAs are long heterogeneous RNAs that regulate gene expression and a variety of signaling pathways involved in cellular homeostasis and development. Several studies have demonstrated that lncRNA is an important class of regulatory molecule that can be targeted to change cellular physiology and function. The expression or dysfunction of lncRNAs is closely related to various hereditary, autoimmune, and metabolic diseases, and tumors. Specifically, recent work has shown that lncRNAs have an important role in kidney pathogenesis. The effective roles of lncRNAs have been recognized in renal ischemia, injury, inflammation, fibrosis, glomerular diseases, renal transplantation, and renal-cell carcinoma. The present review focuses on the emerging role and function of lncRNAs in the pathogenesis of kidney inflammation and fibrosis as novel essential regulators. Although lncRNAs are important players in the initiation and progression of many pathological processes, their role in renal fibrosis remains unclear. This review summarizes the current understanding of lncRNAs in the pathogenesis of kidney fibrosis and elucidates the potential role of these novel regulatory molecules as therapeutic targets for the clinical treatment of kidney inflammation and fibrosis.

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“…Xie et al reported lncRNA H19 overexpression promoted renal fibrosis [70]. Chen et al characterized downregulation of an intergenic lncRNA LINC00963, which suppresses RIF (renal interstitial fibrosis) and OS (oxidative stress) of CRF (chronic renal failure) through activation of the FoxO (forkhead box O) signaling pathway [71]. Zhou et al demonstrated that lncRNA HOTAIR participated in renal interstitial fibrosis through upregulating miR-124 to block Notch1 pathway [72].…”

Section: Renal Fibrosis / Chronic Kidney Diseasementioning

confidence: 99%

Long noncoding RNAs in renal diseases

Liu

Ren

2019

ExRNA

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Long noncoding RNAs (lncRNAs) play critical roles in eukaryotic gene regulation and diseases, rather than being merely transcriptional "noise". Over the past decade, the study of lncRNAs has emerged as a burgeoning field of research and expanded our knowledge of their functions and underlining mechanisms in both normal and malignant cells. However, lncRNAs are still one of the least understood groups of transcripts. Here, we review the classifications and functions of lncRNAs and their roles in renal diseases. This review will provide insights into the roles of lncRNAs in pathogenesis, diagnosis and therapeutics of renal diseases and indications of lncRNAs as potential targets for the treatment of kidney diseases.

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Effects of Long Non-Coding RNA LINC00963 on Renal Interstitial Fibrosis and Oxidative Stress of Rats with Chronic Renal Failure via the Foxo Signaling Pathway

Cited by 50 publications

References 40 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

Potential Roles of Long Noncoding RNAs as Therapeutic Targets in Renal Fibrosis

Long noncoding RNAs in renal diseases

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