Downregulation of lncRNA UCA1 ameliorates the damage of dopaminergic neurons, reduces oxidative stress and inflammation in Parkinson's disease through the inhibition of the PI3K/Akt signaling pathway

Cai, Liang; Tu, Li; Tian, Li; Yang, Xian‐Wen; Ren, Yipin; Gu, Ran; Zhang, Qian; Yao, Huan; Qiu, Xiang; Wang, Qian; Tian, Jing

doi:10.1016/j.intimp.2019.105734

Cited by 69 publications

(41 citation statements)

References 37 publications

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“…While the molecular mechanisms underlying increased expression of UCA1 are not well understood, the antiinflammatory effect of aspirin could be a determining factor for this. As already mentioned, the relationship between UCA1 and inflammatory pathways has been reported in several studies [26,27], and the protective effects of aspirin on colon and lung cancers through modulation of some lncRNAs have previously been suggested [28,29]. Aspirin is known as a nonsteroidal antiinflammatory drug, and it has also been reported that at the antiplatelet activity dose, it can change cyclooxygenase-2 or COX-2 to the antiinflammatory mediator 15-epi-lipoxin.…”

Section: Discussionmentioning

confidence: 86%

Modulation of TNF-α plasma levels in coronary artery disease [CAD] and non-CAD male patients by lncRNA UCA1 and aspirin

Nowrouzi-Sohrabi

Seghatoleslam

Izadpanah

et al. 2020

ARCH BIOL SCI BELGRA

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The aim of this study was to investigate the expression of long non-coding RNA urothelial carcinoma-associated 1 (UCA1) and its role in TNF-? production as one of the main inflammatory cytokines, in peripheral blood mononuclear cells (PBMCs) of patients with coronary artery disease (CAD) and healthy non-CAD (NCAD) individuals as the control group. Fifteen CAD and 15 NCAD individuals were enrolled in the study. UCA1 expression in PBMCs and the plasma concentrations of interleukin (IL)-6, IL-22 and tumor necrosis factor (TNF)-? were assessed by real-time PCR and flow cytometry, respectively. UCA1 expression was not significantly different between the CAD and NCAD groups, however, its level was higher in PBMCs of regular aspirin users of both study groups. Furthermore, aspirin users showed a significantly lower plasma level of TNF-? in comparison to nonaspirin users. In addition, UCA1 expression was negatively correlated with the level of TNF-? in the total sample of the examined population. It seems that the increased levels of UCA1 may be an underlying mechanism for down regulation of TNF-? in aspirin users.

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Section: Discussionmentioning

confidence: 86%

Modulation of TNF-α plasma levels in coronary artery disease [CAD] and non-CAD male patients by lncRNA UCA1 and aspirin

Nowrouzi-Sohrabi

Seghatoleslam

Izadpanah

et al. 2020

ARCH BIOL SCI BELGRA

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“…The GO and KEGG analyses revealed that DE-circRNAs are mainly involved in glutamic synapse, Parkinson's disease, axon guidance, photohadylinositol signaling system, etc. These biological functions and pathways are involved in the pathogenesis of PD [43][44][45][46]. It is suggested that circRNAs may be involved in the pathogenesis of PD.…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Profiling of Circular RNA in Different Brain Regions of Parkinson’s Disease in a Mouse Model

Jia

Zhou

Liu

et al. 2020

IJMS

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Parkinson’s disease (PD) is the second most common neurodegenerative disease and although many studies have been done on this disease, the underlying mechanisms are still poorly understood and further studies are warranted. Therefore, this study identified circRNA expression profiles in the cerebral cortex (CC), hippocampus (HP), striatum (ST), and cerebellum (CB) regions of the 1-methyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model using RNA sequencing (RNA-seq), and differentially expressed circRNA were validated using reverse transcription quantitative real-time PCR (qRT-PCR). Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and competing endogenous RNA (ceRNA) network analyses were also performed to explore the potential function of circRNAs. The results show that, compared with the control group, 24, 66, 71, and 121 differentially expressed circRNAs (DE-circRNAs) were found in the CC, HP, ST, and CB, respectively. PDST vs. PDCB, PDST vs. PDHP, and PDCB vs. PDHP groups have 578, 110, and 749 DE-circRNAs, respectively. Then, seven DE-cirRNAs were selected for qRT-PCR verification, where the expressions were consistent with the sequencing analysis. The GO and KEGG pathway analyses revealed that these DE-circRNAs participate in several biological functions and signaling pathways, including glutamic synapse, neuron to neuron synapse, cell morphogenesis involved in neuron differentiation, Parkinson’s disease, axon guidance, cGMP-PKG signaling pathway, and PI3K-Akt signaling pathway. Furthermore, the KEGG analysis of the target genes predicted by DE-circRNAs indicated that the target genes predicted by mmu_circRNA_0003292, mmu_circRNA_0001320, mmu_circRNA_0005976, and mmu_circRNA_0005388 were involved in the PD-related pathway. Overall, this is the first study on the expression profile of circRNAs in the different brain regions of PD mouse model. These results might facilitate our understanding of the potential roles of circRNAs in the pathogenesis of PD. Moreover, the results also indicate that the mmu_circRNA_0003292-miRNA-132-Nr4a2 pathway might be involved in the regulation of the molecular mechanism of Parkinson’s disease.

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“…The PI3K/Akt pathway regulates apoptosis during oxidative stress. Studies have shown that activation of the PI3K/Akt pathway protects nerve cells from oxidative stress (44,45). Inhibition of Akt activity makes cells more sensitive to ROS and more susceptible to oxidative damage (46).…”

Section: Discussionmentioning

confidence: 99%

Dimethyl fumarate protects nucleus pulposus cells from inflammation and oxidative stress and delays the intervertebral disc degeneration

et al. 2020

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Lower back pain is a common problem in middle-aged and elderly people, and intervertebral disc degeneration (IVDD) is often the main cause. The present study aimed to explore the effects of dimethyl fumarate (DMF) on inflammation and oxidative stress in the intervertebral disc. C57/BL6 mice were used to construct an IVDD model by tail suspension and daily intraperitoneal injections of 10 mg/kg DMF were administered to analyze the effects of DMF on IVDD. In addition, human nucleus pulposus (NP) cells were cultured and stimulated cells with recombinant human IL-1β and DMF to examine the effects of DMF on inflammation and oxidative stress in NP cells. DMF significantly increased the intervertebral disc height index of mice and inhibited the degradation of the extracellular matrix of mouse NP tissue. In addition, DMF also decreased the expression of inflammatory factors [including IL-6, IL-8, matrix metalloproteinase (MMP)3 and MMP13] in NP cells. In terms of oxidative stress, DMF significantly increased the antioxidative stress response in NP cells and reduced endoplasmic reticulum stress. DMF also increased the activity of the nuclear factor erythroid 2-related factor (Nrf) 2/heme oxygenase (HO)-1 signaling pathway in NP cells and increased the phosphorylation of Akt. DMF also increased the anti-inflammatory and antioxidative ability of NP cells by promoting the activity of the Nrf2/HO-1 and PI3K/Akt signaling pathways, thus delaying IVDD.

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Downregulation of lncRNA UCA1 ameliorates the damage of dopaminergic neurons, reduces oxidative stress and inflammation in Parkinson's disease through the inhibition of the PI3K/Akt signaling pathway

Cited by 69 publications

References 37 publications

Modulation of TNF-α plasma levels in coronary artery disease [CAD] and non-CAD male patients by lncRNA UCA1 and aspirin

Modulation of TNF-α plasma levels in coronary artery disease [CAD] and non-CAD male patients by lncRNA UCA1 and aspirin

Transcriptomic Profiling of Circular RNA in Different Brain Regions of Parkinson’s Disease in a Mouse Model

Dimethyl fumarate protects nucleus pulposus cells from inflammation and oxidative stress and delays the intervertebral disc degeneration

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