Long Noncoding RNA SNHG1 Promotes Neuroinflammation in Parkinson’s Disease via Regulating miR-7/NLRP3 Pathway

Cao, Bingqing; Wang, Tao; Qu, Qing; Tai, Kang; Yang, Qian

doi:10.1016/j.neuroscience.2018.07.019

Cited by 128 publications

(108 citation statements)

References 32 publications

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“…In addition, the ratio of Bax/Bcl‐2 is believed to be a reliable indicator of apoptosis . Interestingly, a previous study showed that the knockdown of NLRP3 protects cells from apoptosis . This finding suggests that Rg1 can inhibit LPS‐induced apoptosis via the TLR4/NF‐κB/NLRP3 axis.…”

Section: Discussionmentioning

confidence: 99%

“…The Toll‐like receptor 4 (TLR4), nuclear factor‐κB (NF‐κB), and NOD‐like receptor 3 (NLRP3) pathways are involved in inflammation and apoptosis . The activation of TLR4 can induce the secretion of inflammatory cytokines, including tumor necrosis factor‐α (TNF‐α), interleukin‐1β (IL‐1β), and IL‐18, which are mediated by NF‐κB .…”

Section: Introductionmentioning

confidence: 99%

“…In addition, the activation of NF‐κB is important for upregulating the expression of the NLR family and the pyrin domain containing 3 (NLRP3) inflammasome . The NLRP3 inflammasome, a complex composed of NLRP3, ASC, and caspase‐1, is one of the best investigated inflammasomes and has been demonstrated to promote the production of proinflammatory cytokines and apoptosis …”

Section: Introductionmentioning

confidence: 99%

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Ginsenoside Rg1 attenuates cardiomyocyte apoptosis and inflammation via the TLR4/NF‐kB/NLRP3 pathway

Luo

Yan

Sun

et al. 2019

J of Cellular Biochemistry

123

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Sepsis‐induced myocardial dysfunction (SIMD) causes high mortality in seriously ill patients. Ginsenoside Rg1 has been proven to have effective anti‐inflammatory and antiapoptotic properties. However, the specific role of Rg1 in SIMD and the molecular mechanism remain unclear. Hence, we aimed to investigate the latent effects of ginsenoside Rg1 against SIMD and explore its underlying mechanisms. Male C57BL/6J mice and neonatal rat cardiomyocytes (NRCMs) were used as in vivo and in vitro models, respectively. Western blot analysis was used to detect the level of protein expression, and reverse transcription polymerase chain reaction was conducted to determine the messenger RNA expression of inflammatory factors. The terminal deoxynucleotidyl transferase‐mediated nick end labeling assay and flow cytometry were used to determine the apoptosis rate. Echocardiography was performed to assess cardiac function. The results showed that Rg1 improved cardiac function and attenuated lipopolysaccharide (LPS)‐induced apoptosis and inflammation in mice. In addition, in NRCMs, Rg1 downregulated the expression of LPS‐induced inflammatory cytokines and reversed the increased expression of Toll‐like receptor 4 (TLR4), nuclear factor‐κB (NF‐κB), and NOD‐like receptor 3 (NLRP3). In addition, treatment with TLR4 small interfering RNA (siRNA), a p‐NF‐κB inhibitor, or NLRP3 siRNA suppressed LPS‐induced apoptosis and inflammation. In conclusion, Rg1 can attenuate LPS‐induced inflammation and apoptosis both in NRCMs and septic mice and restore impaired cardiac function. Moreover, Rg1 may exert its effect via blocking the TLR4/NF‐κB/NLRP3 pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Ginsenoside Rg1 attenuates cardiomyocyte apoptosis and inflammation via the TLR4/NF‐kB/NLRP3 pathway

Luo

Yan

Sun

et al. 2019

J of Cellular Biochemistry

123

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“…SNHG1 has been reported to downregulate microRNA‐7 (miR‐7), an endogenous noncoding RNA that targets NLRP3 inflammasome and modulates neuroinflammation in LPS‐induced BV‐2 microglial cells . Similarly, downregulation of SNHG1 elevates the expression of miR‐7 expression and suppresses activation of microglial NLRP3 inflammasomes in MPTP‐treated mice . Therefore, SNHG1 plays a critical role in the α‐synuclein aggregation and NLRP3 inflammasome‐mediated dopaminergic neuronal loss in the SNpc.…”

Section: Nlrp3 Inflammasome‐mediated Inflammatory Pathways In Pdmentioning

confidence: 99%

Targeting the Microglial NLRP3 Inflammasome and Its Role in Parkinson's Disease

et al. 2019

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Excessive activation of microglia and subsequent release of proinflammatory cytokines play a crucial role in neuroinflammation and neurodegeneration in Parkinson's disease (PD). Components of the nucleotide‐binding oligomerization domain and leucine‐rich‐repeat‐ and pyrin‐domain‐containing 3 inflammasome complex, leucine‐rich‐repeat‐ and pyrin‐domain‐containing 3, caspase‐1, and apoptosis‐associated speck‐like protein containing a CARD, are highly expressed in activated microglia in PD patient brains. Findings suggest that neurotoxins, aggregation of α‐synuclein, mitochondrial reactive oxygen species, and disrupted mitophagy are the key regulators of microglial leucine‐rich‐repeat‐ and pyrin‐domain‐containing 3 inflammasome activation and release of interleukin‐1β and interleukin‐18 caspase‐1‐mediated pyroptotic cell death in the substantia nigra of the brain. Although this evidence suggests the leucine‐rich‐repeat‐ and pyrin‐domain‐containing 3 inflammasome may be a potential drug target for treatment of PD, the exact mechanism of how the microglia sense these stimuli and initiate leucine‐rich‐repeat‐ and pyrin‐domain‐containing 3 inflammasome signaling is unknown. Here, the molecular mechanism and regulation of microglial leucine‐rich‐repeat‐ and pyrin‐domain‐containing 3 inflammasome activation and its role in the pathogenesis of PD are discussed. Moreover, the potential of both endogenous and synthetic leucine‐rich‐repeat‐ and pyrin‐domain‐containing 3 inflammasome modulators, long noncoding RNA, microRNA to develop novel therapeutics to treat PD is presented. Overall, we recommend that the microglial leucine‐rich‐repeat‐ and pyrin‐domain‐containing 3 inflammasome can be a potential target for PD treatment. © 2019 International Parkinson and Movement Disorder Society

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“…and ) or target PD‐associated proteins including leucine‐rich repeat kinase 2 (LRRK2; miR‐205), SNCA (miR‐7, miR‐153), GBA (miR‐22), Parkinson disease protein 7 (PARK7/DJ‐1; miR‐544), and nuclear receptor subfamily 4 group A2 (NR4A2/nuclear receptor related 1 protein (Nurr1); miR‐132) . In addition, several miRNAs, whose expression is enriched in the brain, target PD‐relevant processes, including mammalian target of rapamycin (mTOR) signaling, autophagy, and inflammation or protect neurons from PD stressors such 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) and 6‐hydroxydopamine …”

mentioning

confidence: 99%

Circulating Brain‐Enriched MicroRNAs for Detection and Discrimination of Idiopathic and Genetic Parkinson's Disease

et al. 2019

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Background A minimally invasive test for early detection and monitoring of Parkinson's disease (PD) is a highly unmet need for drug development and planning of patient care. Blood plasma represents an attractive source of biomarkers. MicroRNAs (miRNAs) are conserved noncoding RNA molecules that serve as posttranscriptional regulators of gene expression. As opposed to ubiquitously expressed miRNAs that control house‐keeping processes, brain‐enriched miRNAs regulate diverse aspects of neuron development and function. These include neuron‐subtype specification, axonal growth, dendritic morphogenesis, and spine density. Backed by a large number of studies, we now know that the differential expression of neuron‐enriched miRNAs leads to brain dysfunction. Objectives The aim was to identify subsets of brain‐enriched miRNAs with diagnostic potential for familial and idiopathic PD as well as specify the molecular pathways deregulated in PD. Methods Initially, brain‐enriched miRNAs were selected based on literature review and validation studies in human tissues. Subsequently, real‐time reverse transcription polymerase chain reaction was performed in the plasma of 100 healthy controls and 99 idiopathic and 53 genetic (26 alpha‐synucleinA53T and 27 glucocerebrosidase) patients. Statistical and bioinformatics analyses were carried out to pinpoint the diagnostic biomarkers and deregulated pathways, respectively. Results An explicit molecular fingerprint for each of the 3 PD cohorts was generated. Although the idiopathic PD fingerprint was different from that of genetic PD, the molecular pathways deregulated converged between all PD subtypes. Conclusions The study provides a group of brain‐enriched miRNAs that may be used for the detection and differentiation of PD subtypes. It has also identified the molecular pathways deregulated in PD. © 2019 International Parkinson and Movement Disorder Society

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Long Noncoding RNA SNHG1 Promotes Neuroinflammation in Parkinson’s Disease via Regulating miR-7/NLRP3 Pathway

Cited by 128 publications

References 32 publications

Ginsenoside Rg1 attenuates cardiomyocyte apoptosis and inflammation via the TLR4/NF‐kB/NLRP3 pathway

Ginsenoside Rg1 attenuates cardiomyocyte apoptosis and inflammation via the TLR4/NF‐kB/NLRP3 pathway

Targeting the Microglial NLRP3 Inflammasome and Its Role in Parkinson's Disease

Circulating Brain‐Enriched MicroRNAs for Detection and Discrimination of Idiopathic and Genetic Parkinson's Disease

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