Sonic hedgehog-Dependent Induction of MicroRNA 31 and MicroRNA 150 Regulates <i>Mycobacterium bovis</i> BCG-Driven Toll-Like Receptor 2 Signaling

Ghorpade, Devram Sampat; Holla, Sahana; Kaveri, Srini V.; Bayry, Jagadeesh; Patil, Shripad A.; Balaji, Kithiganahalli Narayanaswamy

doi:10.1128/mcb.01108-12

Cited by 64 publications

(57 citation statements)

References 44 publications

(47 reference statements)

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“…Activation of host signaling pathways upon engagement of surface-or intracellular-expressed PRRs is shown to dictate the immune cell fate. Contribution of signaling pathways like Sonic Hedgehog (30), WNT (31), and NOTCH (41,42) has been deciphered during various bacterial infections as well as during derailed inflammation (43)(44)(45). Here, we found significant contribution of WNT5A during dectin-1-mediated immune responses.…”

Section: Discussionsupporting

confidence: 55%

“…On the other hand, tripartite motif-containing (TRIM) proteins, another component of innate immune cell signaling pathways, are driven for proteosomal degradation by E3 ligases. Interestingly, though microRNA-mediated downregulation of TLR adaptors has been previously reported (43), no studies indicate roles for other posttranslational modifications to regulate their levels and subsequently inhibit TLR responses. In the present context, we observed the role for PIAS-1 and SOCS-1 in downregulating IRAK-1, IRAK-4, and MyD88 in macrophages in response to dectin-1 signaling.…”

Section: Discussionmentioning

confidence: 99%

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The WNT Signaling Pathway Contributes to Dectin-1-Dependent Inhibition of Toll-Like Receptor-Induced Inflammatory Signature

Trinath

Holla

Mahadik

et al. 2014

Molecular and Cellular Biology

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Macrophages regulate cell fate decisions during microbial challenges by carefully titrating signaling events activated by innate receptors such as dectin-1 or Toll-like receptors (TLRs). Here, we demonstrate that dectin-1 activation robustly dampens TLRinduced proinflammatory signature in macrophages. Dectin-1 induced the stabilization of ␤-catenin via spleen tyrosine kinase (Syk)-reactive oxygen species (ROS) signals, contributing to the expression of WNT5A. Subsequently, WNT5A-responsive protein inhibitors of activated STAT (PIAS-1) and suppressor of cytokine signaling 1 (SOCS-1) mediate the downregulation of IRAK-1, IRAK-4, and MyD88, resulting in decreased expression of interleukin 12 (IL-12), IL-1␤, and tumor necrosis factor alpha (TNF-␣). In vivo activation of dectin-1 with pathogenic fungi or ligand resulted in an increased bacterial burden of Mycobacteria, Klebsiella, Staphylococcus, or Escherichia, with a concomitant decrease in TLR-triggered proinflammatory cytokines. All together, our study establishes a new role for dectin-1-responsive inhibitory mechanisms employed by virulent fungi to limit the proinflammatory environment of the host.

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

The WNT Signaling Pathway Contributes to Dectin-1-Dependent Inhibition of Toll-Like Receptor-Induced Inflammatory Signature

Trinath

Holla

Mahadik

et al. 2014

Molecular and Cellular Biology

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“…59 The decisive role for TLR2 in shaping the outcome of infection with several pathogens, including mycobacteria, is well established. 20,[60][61][62] However, contribution of TLR2 responses in modulating autophagy has not been addressed. Present observations could add new insights to the infection-induced TLR2 signaling during inhibition of autophagy.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, signaling via TLR4, as well as TLR7 and TLR8 but not TLR2, an important PRR utilized by pathogens such as Mycobacteria, Shigella, and Listeria, induce autophagy, 17 suggesting that these pathogens might use the TLR2 pathway to escape autophagy. Several reports have shown that TLR2 signaling by Mycobacteria leads to activation of a gamut of pathways like NOTCH1, 18 WNT, 19 SHH (sonic hedgehog) 20 contributing to the differential regulation of the innate immune response and cytokine milieu. 21 Of note, a recent study reveals the inhibitory effects of HH signaling on autophagy.…”

Section: Introductionmentioning

confidence: 99%

“…3A and B), strongly advocates a role for posttranscriptional regulatory mechanisms like those mediated by miRNAs. Data from a miRNA microarray 20 together with extensive bioinformatic analysis (TargetScan, miRanda, miRWalk and RNAhybrid) identified Ppp2r5a as a potential target for Mir155 and Mir31. The target sites located at the residues spanning from 1022 to 1028 (for Mir155) and 960 to 967 (for Mir31) in Ppp2r5a mRNA were identified as critical for miRNA-3′UTR interactions (Fig.…”

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Selective inhibition of IFNG-induced autophagy byMir155- andMir31-responsive WNT5A and SHH signaling

et al. 2013

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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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Sonic hedgehog-Dependent Induction of MicroRNA 31 and MicroRNA 150 Regulates Mycobacterium bovis BCG-Driven Toll-Like Receptor 2 Signaling

Cited by 64 publications

References 44 publications

The WNT Signaling Pathway Contributes to Dectin-1-Dependent Inhibition of Toll-Like Receptor-Induced Inflammatory Signature

The WNT Signaling Pathway Contributes to Dectin-1-Dependent Inhibition of Toll-Like Receptor-Induced Inflammatory Signature

Selective inhibition of IFNG-induced autophagy byMir155- andMir31-responsive WNT5A and SHH signaling

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

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