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The role of the microRNA-146a/complement factor H/interleukin-1?-mediated inflammatory loop circuit in the perpetuate inflammation of chronic temporal lobe epilepsy.

ABSTRACT: Increasing evidence indicates that neuroinflammation plays a crucial role in the pathogenesis of temporal lobe epilepsy (TLE). However, it is unclear how the perpetuate inflammation develops. Some recent studies have suggested the possible involvement of microRNA-146a (miR-146a) in the modulation of inflammatory signaling occurring in TLE. To understand how miR-146a modulates inflammatory signaling in TLE, we investigated the role of interleukin-1? (IL-1?), miR-146a and human complement factor H (CFH) in the perpetuate inflammation in rat models of chronic TLE and U251 cells. We found that enhancive miR-146a could upregulate the expression of IL-1? and downregulate the expression of CFH, whereas reductive miR-146a could downregulate the expression of IL-1? and upregulate the expression of CFH, in hippocampi of chronic TLE rat models. Meanwhile, enhancive miR-146a could increase the abnormal wave forms in the chronic TLE rat models. Additionally, enhancive IL-1? could feedback downregulate the expression of CFH, upregulate the expression of miR-146a and increase the abnormal wave forms in chronic TLE rat models. After CFH gene knockdown in U251 cells, enhancive miR-146a did not upregulate the expression of IL-1?. In summary, this study shows that enhancive miR-146a can upregulate the inflammatory factor IL-1? in chronic TLE by downregulating CFH, and that upregulation of IL-1? plays an important feedback-regulating role in the expression of miR-146a and CFH, forming a miR-146a-CFH-IL-1? loop circuit that initiates a cascade of inflammation and then leads to the perpetuate inflammation in TLE. Therefore, modulation of the miR-146a-CFH-IL-1? loop circuit could be a novel therapeutic target for TLE.

SUBMITTER: Li TR

PROVIDER: S-EPMC5897725 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature

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The role of the microRNA-146a/complement factor H/interleukin-1β-mediated inflammatory loop circuit in the perpetuate inflammation of chronic temporal lobe epilepsy.

Li Tao-Ran TR Jia Yan-Jie YJ Ma Chao C Qiu Wen-Ying WY Wang Qun Q Shao Xiao-Qiu XQ Lv Rui-Juan RJ

Disease models & mechanisms 20180323 3

Increasing evidence indicates that neuroinflammation plays a crucial role in the pathogenesis of temporal lobe epilepsy (TLE). However, it is unclear how the perpetuate inflammation develops. Some recent studies have suggested the possible involvement of microRNA-146a (miR-146a) in the modulation of inflammatory signaling occurring in TLE. To understand how miR-146a modulates inflammatory signaling in TLE, we investigated the role of interleukin-1β (IL-1β), miR-146a and human complement factor H ...[more]

PMID: 29590637

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Project description:ObjectiveTo identity phenotypes of self-reported symptoms of psychopathology and their correlates in patients with temporal lobe epilepsy (TLE).Method96 patients with TLE and 82 controls were administered the Symptom Checklist 90-Revised (SCL-90-R) to characterize emotional-behavioral status. The nine symptom scales of the SCL-90-R were analyzed by unsupervised machine learning techniques to identify latent TLE groups. Identified clusters were contrasted to controls to characterize their association with sociodemographic, clinical epilepsy, neuropsychological, psychiatric, and neuroimaging factors.ResultsTLE patients as a group exhibited significantly higher (abnormal) scores across all SCL-90-R scales compared to controls. However, cluster analysis identified three latent groups: (1) unimpaired with no scale elevations compared to controls (Cluster 1, 42% of TLE patients), (2) mild-to-moderate symptomatology characterized by significant elevations across several SCL-90-R scales compared to controls (Cluster 2, 35% of TLE patients), and (3) marked symptomatology with significant elevations across all scales compared to controls and the other TLE phenotype groups (Cluster 3, 23% of TLE patients). There were significant associations between cluster membership and demographic (education), clinical epilepsy (perceived seizure severity, bitemporal lobe seizure onset), and neuropsychological status (intelligence, memory, executive function), but with minimal structural neuroimaging correlates. Concurrent validity of the behavioral phenotype grouping was demonstrated through association with psychiatric (current and lifetime-to-date DSM IV Axis 1 disorders and current treatment) and quality-of-life variables.SignificanceSymptoms of psychopathology in patients with TLE are characterized by a series of discrete phenotypes with accompanying sociodemographic, cognitive, and clinical correlates. Similar to cognition in TLE, machine learning approaches suggest a developing taxonomy of the comorbidities of epilepsy.

Dataset Information

The role of the microRNA-146a/complement factor H/interleukin-1?-mediated inflammatory loop circuit in the perpetuate inflammation of chronic temporal lobe epilepsy.

Publications

The role of the microRNA-146a/complement factor H/interleukin-1β-mediated inflammatory loop circuit in the perpetuate inflammation of chronic temporal lobe epilepsy.

Similar Datasets

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