scholarly journals Association of circulating long non‐coding RNA HULC expression with disease risk, inflammatory cytokines, biochemical index levels, severity‐assessed scores, and mortality of sepsis

2020 ◽  
Author(s):  
Haiyan Wang ◽  
Qiang Feng ◽  
Yiping Wu ◽  
Lingxiang Feng ◽  
Haiyan Yuan ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Disease Risk ◽  
Biochemical Index ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals A long-non-coding RNA, LINC00473, confers the human adipose tissue thermogenic phenotype through enhanced cAMP responsiveness

2018 ◽  
Author(s):  
Khanh-Van Tran ◽  
Cecilie Nandrup-Bus ◽  
Tiffany DeSouza ◽  
Ricardo Soares ◽  
Naja Zenius Jespersen ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Adipose Tissue ◽  
Disease Risk ◽  
Human Adipose Tissue ◽  
Non Coding Rna ◽  
Highly Correlated ◽  
Thermogenic Adipocytes ◽  
The Many ◽  
External Stimuli ◽  
Long Non Coding Rna

SummarySpecialized adipocytes localized in distinct depots mediate the many physiological functions of adipose tissue. In humans, paucity of thermogenic adipocytes correlates with high metabolic disease risk, raising much interest in the mechanisms by which these cells arise. Here we report molecular signatures associated with adipocyte development in different human depots and identify a long non-coding RNA, LINC00473, as the transcript most closely associated with enrichment of thermogenic adipocytes. LINC00473 expression is low in subjects with obesity or type-2 diabetes and is highly correlated with cAMP signaling and mitochondrial oxidative phosphorylation pathways. LINC00473 is localized in the nucleus and the cytoplasm, and its knockdown impairs induction of UCP1 and mitochondrial respiration. These results reveal that depot-enriched genes that modulate responsiveness to external stimuli, specifically LINC00473, are important determinants of the adipose tissue thermogenic phenotype, and potential targets for metabolic disease therapy.

scholarly journals Knockdown of Long Non-Coding RNA RP11-445H22.4 Alleviates LPS-Induced Injuries by Regulation of MiR-301a in Osteoarthritis

2018 ◽  
Vol 45 (2) ◽  
pp. 832-843 ◽  
Author(s):  
Taitao Sun ◽  
Jian Yu ◽  
Liang Han ◽  
Shuo Tian ◽  
Bin Xu ◽  
...  
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Inflammatory Cytokines ◽  
Luciferase Reporter ◽  
Signal Pathways ◽  
Related Factors ◽  
Human Cartilage ◽  
Non Coding Rna ◽  
Tnf Α ◽  
Long Non Coding Rna

Background/Aims: Several long non-coding RNAs (lncRNAs) play vital roles in osteoarthritis (OA), whereas the role of lncRNA RP11-445H22.4 in OA remains unclear. The study aimed to investigate the effect of lncRNA RP11-445H22.4 on lipopolysaccharide (LPS)-induced cell viability, apoptosis and inflammatory injury of OA. Methods: The expression of RP11-445H22.4, miR-301a and CXCR4 in human cartilage ATDC5 cells were altered by transfection, and then cells were exposed to 5 µg/ml LPS for 12 h. Then cell viability, apoptosis, apoptosis-related factors and inflammatory cytokines were analyzed by CCK-8, flow cytometry, western blot, RT-qPCR and ELISA, respectively. Dual-luciferase reporter assay was performed to assess the binging sites of RP11-445H22.4 and miR-301a. The signal pathways of NF-κB and MAPK/ ERK were determined by western blot. Results: LPS reduced cell viability, increased apoptosis and stimulated release of IL-1β, IL-6, IL-8 and TNF-α. However, RP11-445H22.4 inhibition significantly rescued LPS-induced injuries by promoting cell viability, suppressing apoptosis and inflammatory cytokines secretions in ATDC5 cells. In addition, miR-301a directly bound to RP11-445H22.4, and suppression of miR-301a inversed the effects of RP11-445H22.4 inhibition. Furthermore, CXCR4 was a direct target of miR-301a, and CXCR4 silencing increased cell viability, decreased apoptosis and inflammatory cytokines secretions in LPS-treated ATDC5 cells. Besides, we found that CXCR4 silencing blocked LPS-activated NF-κB and MAPK/ERK pathways. Conclusions: The study indicated that lncRNA RP11-445H22.4-miR-301a-CXCR4 axis played an important role in cartilage ATDC5 cells and provided a theoretical basis of lncRNA RP11-445H22.4 in OA.

scholarly journals Downregulation of long non-coding RNA SNHG7 protects against inflammation and apoptosis in Parkinson's disease model by targeting miR-425-5p/TRAF5/NF-κB axis

2020 ◽  
Author(s):  
Shan Yu ◽  
Xueshibojie Liu ◽  
Duo Yu ◽  
Changyong E ◽  
Jinghui Yang
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Western Blot ◽  
Inflammatory Cytokines ◽  
Neuronal Apoptosis ◽  
Rt Pcr ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
And Oxidative Stress

Abstract Background Accumulated evidence has established that long non-coding RNA (lncRNA) is involved in the progress of Parkinson's disease (PD). SNHG7, a novel lncRNA, has been found to play a key role in tumorigenesis. However, the SNHG7 expression and its functional effects on PD remain uncharted. Methods RT-PCR was used to detect the expression of SNHG7, miR-425-5p and inflammatory cytokines in the plasma of PD patients and the healthy controls. Rotenone (Rot) was adopted to construct PD models in SD rats and SH-SY5Y cells, respectively. Gain- and loss- of functions of SNHG7 or miR-425-5p were conducted. The expression levels of Caspase3, tyrosine hydroxylase (TH), Iba1 in SD rat striatum was measured via immunohistochemistry and Western blot. Additionally, the expressions of inflammatory cytokines (IL-1β, IL-6, TNF-α) and oxidative stress factors (MDA, SOD, GSH-PX) in the brain tissues were examined using RT-PCR and ELISA. Moreover, the protein levels of TRAF5, I-κB, NF-κB, HO-1, Nrf2 were detected via Western blot. Bioinformatics was applied to predict the targeting relationship between SNHG7, miR-425-5p and TRAF5. Dual luciferase activity assay and RNA immunoprecipitation (RIP) assays were carried out to verify their interactions. Results SNHG7 was found up-regulated in PD patients while miR-425-5p expression was down-regulated (compared to healthy donors). Meanwhile, SNHG7 level was positively correlated with the level of inflammatory cytokines in PD patients. Functional experiments confirmed that SNHG7 downregulation or miR-425-5p overexpression attenuated neuronal apoptosis in the Rot-mediated PD model, TH-positive cell loss and microglia activation by mitigating inflammation and oxidative stress. Mechanistically, SNHG7 served as a competitive endogenous RNA (ceRNA) by sponging miR-425-5p and promoted TRAF5 mediated inflammation and oxidative stress. Conclusion Inhibition of SNHG7 ameliorated neuronal apoptosis in PD through relieving miR-425-5p/TRAF5/NF-κB signaling pathway modulated inflammation and oxidative stress.

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