MicroRNA-31 Reduces the Motility of Proinflammatory T Helper 1 Lymphocytes

Bardua, Markus; Haftmann, Claudia; Westendorf, Kerstin; Buttgereit, Antje; Tran, Cam Loan; McGrath, Mairi; Weber, Melanie; Lehmann, Katrin; Addo, Richard; Heinz, Gitta Anne; Stittrich, Anna-Barbara; Maschmeyer, Patrick; Radbruch, Helena; Lohoff, Michael; Chang, Hyun‐Dong; Radbruch, Andreas; Mashreghi, Mir‐Farzin

doi:10.3389/fimmu.2018.02813

Cited by 15 publications

(10 citation statements)

References 74 publications

(126 reference statements)

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“…Isolated long-lived PCs from the bone marrow were cultured in Accell Medium with 2 μM siRNA or scr control ( Bardua et al., 2018 ; Haftmann et al., 2015 ) and 100 ng/ml multimeric APRIL. After 1 hour RMI1640 medium supplemented with 5% FCS, 200 U/ml Penicillin, 200 μg/ml streptomycin0.2% β-Mercaptoethanol, 50 mM HEPES buffer was added to the cells.…”

Section: Methodsmentioning

confidence: 99%

Stromal Cell-Contact Dependent PI3K and APRIL Induced NF-κB Signaling Prevent Mitochondrial- and ER Stress Induced Death of Memory Plasma Cells

et al. 2020

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Summary The persistence of long-lived memory plasma cells in the bone marrow depends on survival factors available in the bone marrow, which are provided in niches organized by stromal cells. Using an ex vivo system in which we supply the known survival signals, direct cell contact to stromal cells, and the soluble cytokine a proliferation-inducing ligand (APRIL), we have elucidated the critical signaling pathways required for the survival of long-lived plasma cells. Integrin-mediated contact of bone marrow plasma cells with stromal cells activates the phosphatidylinositol 3-kinase (PI3K) signaling pathway, leading to critical inactivation of Forkhead-Box-Protein O1/3 (FoxO1/3) and preventing the activation of mitochondrial stress-associated effector caspases 3 and 7. Accordingly, inhibition of PI3K signaling in vivo ablates bone marrow plasma cells. APRIL signaling, by the nuclear factor κB (NF-κB) pathway, blocks activation of the endoplasmic-reticulum-stress-associated initiator caspase 12. Thus, stromal-cell-contact-induced PI3K and APRIL-induced NF-κB signaling provide the necessary and complementary signals to maintain bone marrow memory plasma cells.

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Section: Methodsmentioning

confidence: 99%

Stromal Cell-Contact Dependent PI3K and APRIL Induced NF-κB Signaling Prevent Mitochondrial- and ER Stress Induced Death of Memory Plasma Cells

et al. 2020

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“…Previous literatures found that circRNAs were abundant in microRNAs binding sites and exhibited regulatory functions on genes expressions via sponging microRNAs and altering microRNAs levels . MicroRNA‐31 (miR‐31) is a noted inflammation‐related microRNA, which joins in the modulation of inflammatory response in many human diseases . Weldon et al reported that miR‐31 contributed to modulation of lung inflammation via changing cathepsin S activity .…”

Section: Introductionmentioning

confidence: 99%

Retracted: Circular RNA ANKRD36 attends to lipopolysaccharide‐aroused MRC‐5 cell injury via regulating microRNA‐31‐3p

2019

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Background Some circular RNAs (circRNAs) are reported to attend to the pathogenesis of pneumonia. This study tested the impact of circRNA ankyrin repeat domain 36 (circANKRD36) on human embryonic lung fibroblast MRC‐5 cell injury irritated by lipopolysaccharide (LPS). Methods After LPS irritation, viability, apoptosis, ROS, protein, and cytokines, along with circANKRD36 were tested by CCK‐8, Annexin V‐FITC, DCFH‐DA, and ELISA or Western blot. si‐circANKRD36 and microRNA‐31‐3p/5p (miR‐31‐3p/5p) inhibitor were applied to silence circANKRD36 and miR‐31‐3p/5p. miR‐31‐3p/5p mimic was utilized to upregulate miR‐31‐3p/5p. RT‐qPCR was used to detect miRNAs. The relationship between miRNAs and MyD88 or IL‐34 was analyzed by luciferase activity reporter assay. Results LPS aroused a decrease in viability, increases in apoptosis, ROS, and IL‐6, IL‐8, and TNF‐α, along with circANKRD36, and activation of NF‐κB pathway. Silencing circANKRD36 weakened the above‐mentioned influences of LPS. Moreover, silencing circANKRD36 hoisted miR‐31‐3p expression. Silencing miR‐31‐3p mitigated the impacts of circANKRD36 silence on LPS‐irritated MRC‐5 cells. Besides, MyD88 was a downstream target of miR‐31‐3p, and 3′UTR of IL‐34 mRNA was targeted by miR‐31‐5p. LPS induced the accumulation of MyD88. Silencing MyD88 was constructive to maintain cell viability, retard apoptosis and inhibit adverse oxidation and inflammation. Conclusion This research verified that silencing circANKRD36 could weaken LPS‐irritated MRC‐5 cell injury via regulating miR‐31/MyD88‐mediated repression of NF‐κB pathway.

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“…Using microarray and quantitative real-time polymerase chain reaction (PCR) analysis to measure miRNA expression and applying UFP-512, a potent and specific DOR agonist, to activate DOR in Sprague-Dawley rats (33)(34)(35)(36), we found that some miRNAs significantly change their expression upon DOR activation in the brain under normoxic condition, and such modulation becomes more profound in hypoxic/ischemic conditions, especially after a prolonged period. For instance, DOR activation did not alter the brain miR-31 expression under normoxic condition, but it led to a 50% increase in miR-31 levels after 1-day hypoxic exposure, suggesting that DOR activation up-regulates miR-31 in hypoxia (34), thus inhibiting proinflammatory T H 1 cells and cell glucose metabolism (124,125). In the same animal model, DOR activation reduced the levels of miR-347 and miR-466b in the cortex after prolonged hypoxia as compared to DOR activation in normoxic animals (34).…”

Section: δ-Opioid Receptor-induced Alterations In Mirna Expression Inmentioning

confidence: 99%

δ-Opioid Receptors, microRNAs, and Neuroinflammation in Cerebral Ischemia/Hypoxia

Chen

Wang

et al. 2020

Front. Immunol.

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Hypoxia and ischemia are the main underlying pathogenesis of stroke and other neurological disorders. Cerebral hypoxia and/or ischemia (e.g., stroke) can lead to neuronal injury/death and eventually cause serious neurological disorders or even death in the patients. Despite knowing these serious consequences, there are limited neuroprotective strategies against hypoxic and ischemic insults in clinical settings. Recent studies indicate that microRNAs (miRNAs) are of great importance in regulating cerebral responses to hypoxic/ischemic stress in addition to the neuroprotective effect of the δ-opioid receptor (DOR). Moreover, new discovery shows that DOR can regulate miRNA expression and inhibit inflammatory responses to hypoxia/ischemia. We, therefore, summarize available data in current literature regarding the role of DOR and miRNAs in regulating the neuroinflammatory responses in this article. In particular, we focus on microglia activation, cytokine production, and the relevant signaling pathways triggered by cerebral hypoxia/ischemia. The intent of this review article is to provide a novel clue for developing new strategies against neuroinflammatory injury resulting from cerebral hypoxia/ischemia.

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MicroRNA-31 Reduces the Motility of Proinflammatory T Helper 1 Lymphocytes

Cited by 15 publications

References 74 publications

Stromal Cell-Contact Dependent PI3K and APRIL Induced NF-κB Signaling Prevent Mitochondrial- and ER Stress Induced Death of Memory Plasma Cells

Stromal Cell-Contact Dependent PI3K and APRIL Induced NF-κB Signaling Prevent Mitochondrial- and ER Stress Induced Death of Memory Plasma Cells

Retracted: Circular RNA ANKRD36 attends to lipopolysaccharide‐aroused MRC‐5 cell injury via regulating microRNA‐31‐3p

δ-Opioid Receptors, microRNAs, and Neuroinflammation in Cerebral Ischemia/Hypoxia

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