MiR-214-3p exacerbates kidney damages and inflammation induced by hyperlipidemic pancreatitis complicated with acute renal injury

Yan, Zhaopeng; Zhang, Bin; Gong, Xiaoying; Ren, Jiangyue; Wang, Rui

doi:10.1016/j.lfs.2019.117118

Cited by 37 publications

(28 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In cells expressing high levels of EGFR, ERRFI1 acts as a negative regulator of EGFR. [12] In addition, studies on uterine epithelial cells demonstrate that ERRFI1 has a negative regulatory effect on signal transducer and activator of transcription 3 (STAT3) phosphorylation. [13] STAT3 inducing oxidative stress and inflammation in cisplatin-induced AKI has been confirmed.…”

Section: Introductionmentioning

confidence: 99%

A novel role of the miR‐152‐3p/ERRFI1/STAT3 pathway modulates the apoptosis and inflammatory response after acute kidney injury

Zhang

Huo

et al. 2020

J Biochem & Molecular Tox

View full text Add to dashboard Cite

Acute kidney injury (AKI) is one of the most common and serious complications in the development of sepsis. Many microRNAs are closely related to the occurrence, development, and prognosis of sepsis AKI (but the effect and mechanism of miR‐152‐3p in it is unclear). Meanwhile, the ERBB receptor feedback inhibitor 1 (ERRFI1) has a negative regulatory effect on signal transducer and activator of transcription 3 (STAT3) phosphorylation on uterine epithelial cells. But, the relationship between miR‐152‐3p and renal function, inflammatory factors, prognosis in AKI, and the mechanism is not clear. Analyzing sepsis‐induced AKI rats and the cell model, our results revealed that miR‐152‐3p was upregulated in septic AKI patients and positively correlated with serum creatinine, urea nitrogen, interleukin 1β (IL‐1β) and tumor necrosis factor α (TNF‐α). Downregulation of miR‐152‐3p with the inhibitor could dramatically attenuate caspase‐3, bromodeoxyuridine and IL‐1β, and TNF‐α in the AKI rats' model. Furthermore, downregulation of miR‐152‐3p attenuated lipopolysaccharide‐induced apoptosis and inflammatory response in HK‐2 and HEK293 cells. To further explore the mechanisms, we found ERRFI1 was appreciably downregulated and STAT3 was upregulated in AKI, whereas ERRFI1 was radically upregulated and STAT3 was greatly downregulated after the addition of miR‐152‐3p inhibitor, no matter in vivo or in vitro. Summarily, our study confirmed that miR‐152‐3p could promote the expression of STAT3 by targeting ERRFI1, aggravate cell apoptosis and inflammatory response, and thereby aggravate kidney injury in sepsis AKI.

show abstract

Section: Introductionmentioning

confidence: 99%

A novel role of the miR‐152‐3p/ERRFI1/STAT3 pathway modulates the apoptosis and inflammatory response after acute kidney injury

Zhang

Huo

et al. 2020

J Biochem & Molecular Tox

View full text Add to dashboard Cite

show abstract

“…Recently, accumulating reports suggested that certain LncRNAs and miRNAs were associated with pathogenesis and development of AKI (Brandenburger et al, 2018;Brandenburger and Lorenzen, 2020;Yan et al, 2020). Our results showed that lncRNA H19 was significantly increased while miR-130a was decreased in HK-2 cells under H/R treatment.…”

Section: Discussionmentioning

confidence: 46%

Long Non-coding RNA H19 Augments Hypoxia/Reoxygenation-Induced Renal Tubular Epithelial Cell Apoptosis and Injury by the miR-130a/BCL2L11 Pathway

Yuan

Li²,

Chu

et al. 2021

Front. Physiol.

View full text Add to dashboard Cite

Acute kidney injury (AKI) is a severe kidney disease defined by partial or abrupt loss of renal function. Emerging evidence indicates that non-coding RNAs (ncRNAs), particularly long non-coding RNAs (lncRNAs), function as essential regulators in AKI development. Here we aimed to explore the underlying molecular mechanism of the lncRNA H19/miR-130a axis for the regulation of inflammation, proliferation, and apoptosis in kidney epithelial cells. Human renal proximal tubular cells (HK-2) were induced by hypoxia/reoxygenation to replicate the AKI model in vitro. After treatment, the effects of LncRNA H19 and miR-130a on proliferation and apoptosis of HK-2 cells were investigated by CCK-8 and flow cytometry. Meanwhile, the expressions of LncRNA H19, miR-130a, and inflammatory cytokines were detected by qRT-PCR, western blot, and ELISA assays. The results showed that downregulation of LncRNA H19 could promote cell proliferation, inhibit cell apoptosis, and suppress multiple inflammatory cytokine expressions in HK-2 cells by modulating the miR-130a/BCL2L11 pathway. Taken together, our findings indicated that LncRNA H19 and miR-130a might represent novel therapeutic targets and early diagnostic biomarkers for the treatment of AKI.

show abstract

“…Upregulation of miR-214-3p inhibits PTEN expression, but increases the level of P-Akt in HP kidneys which may be a possible mechanism for inducing severe symptoms of pancreatitis, and exacerbates HP-induced pathological changes, kidney and pancreas damage, and fibrosis. Therefore, using miR-214-3p as target for the treatment of acute renal injury of HP provides a potential and effective method for the clinic (Yan Z et al, 2020). Manuscript to be reviewed al., 2020).…”

Section: Mir-214 and Inflammationmentioning

confidence: 99%

Peer Review #2 of "Immune function of miR-214 and its application prospects as molecular marker (v0.1)"

2021

View full text Add to dashboard Cite

MicroRNAs are a class of evolutionary conserved non-coding small RNAs that play key regulatory roles at the post-transcriptional level. In recent years, studies have shown that miR-214 plays an important role in regulating several biological processes such as cell proliferation and differentiation, tumorigenesis, inflammation and immunity, and has become a hotspot in the miRNA field. In this review, the regulatory functions of miR-214 in the proliferation, differentiation and functional activities of immune-related cells, such as dendritic cells, T cells and NK cells, were briefly reviewed. Also, the mechanisms of miR-214 involved in tumor immunity, inflammatory regulation and antivirus were discussed. Finally, the value and application prospects of miR-214 as a molecular marker in inflammation and tumor related diseases were analyzed briefly. We hope it can provide reference for further study on the mechanism and application of miR-214.

show abstract

MiR-214-3p exacerbates kidney damages and inflammation induced by hyperlipidemic pancreatitis complicated with acute renal injury

Cited by 37 publications

References 39 publications

A novel role of the miR‐152‐3p/ERRFI1/STAT3 pathway modulates the apoptosis and inflammatory response after acute kidney injury

A novel role of the miR‐152‐3p/ERRFI1/STAT3 pathway modulates the apoptosis and inflammatory response after acute kidney injury

Long Non-coding RNA H19 Augments Hypoxia/Reoxygenation-Induced Renal Tubular Epithelial Cell Apoptosis and Injury by the miR-130a/BCL2L11 Pathway

Peer Review #2 of "Immune function of miR-214 and its application prospects as molecular marker (v0.1)"

Contact Info

Product

Resources

About