MicroRNA-155 induces autophagy in osteoclasts by targeting transforming growth factor β-activated kinase 1-binding protein 2 upon lipopolysaccharide stimulation

Sul, Ok-Joo; Sung, You-Bin; Rajasekaran, Monisha; Ke, Ke; Yu, Rina; Back, Sung-Hoon; Choi, Hye-Seon

doi:10.1016/j.bone.2018.08.014

Cited by 31 publications

(37 citation statements)

References 39 publications

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“…The relevance of miRNAs in interplay between autophagy and osteoclastogenesis was revealed in a lipopolysaccharide-induced inflammatory condition. It was shown that miR-155 directly induces autophagy in osteoclasts by regulating their differentiation and activity by targeting TAB2 (TGF-β-activated kinase 1-binding protein 2) [ 79 ].…”

Section: Autophagy In Osteoclast Differentiation/functionmentioning

confidence: 99%

The Role of Autophagy in Osteoclast Differentiation and Bone Resorption Function

et al. 2020

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Autophagy is an evolutionary conserved and highly regulated recycling process of cellular wastes. Having a housekeeping role, autophagy through the digestion of domestic cytosolic organelles, proteins, macromolecules, and pathogens, eliminates unnecessary materials and provides nutrients and energy for cell survival and maintenance. The critical role of autophagy and autophagy-related proteins in osteoclast differentiation, bone resorption, and maintenance of bone homeostasis has previously been reported. Increasing evidence reveals that autophagy dysregulation leads to alteration of osteoclast function and enhanced bone loss, which is associated with the onset and progression of osteoporosis. In this review, we briefly consolidate the current state-of-the-art technology regarding the role of autophagy in osteoclast function in both physiologic and pathologic conditions to have a more general view on this issue.

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Section: Autophagy In Osteoclast Differentiation/functionmentioning

confidence: 99%

The Role of Autophagy in Osteoclast Differentiation and Bone Resorption Function

et al. 2020

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“…In animal models, lipopolysaccharide (LPS) treatment induces systemic inflammation along with severe bone loss via the activity of OCs [ 8 , 9 , 10 ]. In vitro, LPS has been reported to enhance the differentiation, survival, and function of OCs [ 11 , 12 , 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Dauricine Protects from LPS-Induced Bone Loss via the ROS/PP2A/NF-κB Axis in Osteoclasts

et al. 2020

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Dauricine (DAC), an isoquinoline alkaloid, exhibits anti-inflammatory activity. We hypothesized that DAC may prevent the inflammatory bone loss induced by lipopolysaccharide (LPS). LPS-induced bone loss was decreased by DAC in female C57BL/6J mice as evaluated by micro-computerized tomography (μCT) analysis. In vivo tartrate-resistant acid phosphatase (TRAP) staining showed that the increased number of osteoclasts (OCs) in LPS-treated mice was attenuated by DAC, indicating that DAC exhibited bone sparing effects through acting on OCs. DAC also decreased the differentiation and activity of OCs after LPS stimulation in vitro. LPS-induced cytosolic reactive oxygen species (cROS) oxidized PP2A, a serine/threonine phosphatase, leading to the activation of IKKα/β, followed by the nuclear localization of p65. DAC decreased LPS-induced ROS, resulting in the recovery of the activity of PP2A by reducing its oxidized form. Consequently, DAC reduced the phosphorylation of IKKα/β to block the nuclear localization of p65, which decreased NF-κB activation. Taken together, DAC reduced the differentiation and activity of OCs by decreasing ROS via the ROS/PP2A/NF-κB axis, resulting in protection from LPS-induced bone loss. We have demonstrated that LPS-induced bone loss was inhibited by DAC via its action on OCs, implying the therapeutic potential of DAC against inflammatory bone loss.

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“…2a-c) These data suggest that autophagy plays a role as a negative regulator of in ammation by regulating the expression of in ammatory cytokines.MiR-155 Is Involved in the Cytokine Production of DCs Induced by Dysfunctional AutophagyEarlier we showed that the expression of miR-155 was decreased in DCs from active BD patients [8]. Moreover, miR-155 has been reported to be involved in autophagy regulation [17,[25][26][27]. A further experiment was carried out to investigate if miR-155 was associated with cytokine production by DCs induced by dysfunctional autophagy.…”

mentioning

confidence: 79%

“…[8] It has also been reported that the expression of miR-155 was increased or decreased in various diseases and was involved in the development of these diseases by regulating autophagy. [17,19,32,33] In view of the aforementioned reports, we next investigated whether miR-155 exerted its effects on cytokine production by DCs via the process of autophagy. To answer this question, an experiment with miR-155 mimic transfection was performed.…”

Section: Discussionmentioning

confidence: 99%

“…Our results are in agreement with previous studies that showed that miR-155 promoted autophagy via a decrease in TAB2 expression thereby stimulating osteoclast formation. [17] The Akt/mTOR pathway is one of the most common signaling pathways involved in the control of autophagy. [34,35] Rapamycin, as the inhibitor of mTOR, has been shown to alleviate in ammation of the retina.…”

Section: Discussionmentioning

confidence: 99%

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Decreased MicroRNA-155 in Behcet’s disease leads to defective control of autophagy thereby stimulating excessive proinflammatory cytokine production

Liang

Zhou

Feng

et al. 2020

Preprint

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Background: Earlier we reported that the microRNA (miR)-155 expression in dendritic cells (DCs) from Behcet’s disease (BD) patients was decreased and affected cytokine production of DCs. In this study, we investigated the mechanisms whereby miR-155 regulates cytokine production by DCs.Methods: The formation of autophagosomes in DCs was detected by transmission electron microscopy. Western blotting was used to detect the protein levels of LC3, Beclin-1, P62, p-mTOR and p-Akt in DCs. TNF-α, IL-6 and IL-1β expression were investigated by ELISA. MiR-155 mimics were transfected to DCs to evaluate its effects on autophagy and cytokine production. RNA interference was used to downregulate the expression of TAB2.Results: The formation of autophagosomes was found in DCs of active BD patients. The expressions of LC3-Ⅱ, Beclin-1, P62, IL-6, IL-1β and TNF-α were significantly increased in DCs of active BD patients compared to that of healthy controls. The autophagy promoter (3-MA) and inhibitor (rapamycin) significantly decreased or increased the expression of TNF-α, IL-6 and IL-1β by DCs. The expression of LC3-Ⅱand Beclin-1 were significantly increased, but the expression of P62 proteins was decreased in DCs transfected with miR-155 mimics or after TAB2 was downregulated. The expression of TNF-α, IL-6 and IL-1β were decreased in DCs after miR-155 was upregulated or TAB2 was downregulated. The ratios of p-Akt/Akt and p-mTOR/mTOR were decreased in DCs after miR-155 was upregulated.Conclusions: These results suggest that miR-155 affects the production of TNF-α, IL-6 and IL-1β by DCs through activation of the Akt/mTOR signaling pathway and by affecting the process of autophagy.

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MicroRNA-155 induces autophagy in osteoclasts by targeting transforming growth factor β-activated kinase 1-binding protein 2 upon lipopolysaccharide stimulation

Cited by 31 publications

References 39 publications

The Role of Autophagy in Osteoclast Differentiation and Bone Resorption Function

The Role of Autophagy in Osteoclast Differentiation and Bone Resorption Function

Dauricine Protects from LPS-Induced Bone Loss via the ROS/PP2A/NF-κB Axis in Osteoclasts

Decreased MicroRNA-155 in Behcet’s disease leads to defective control of autophagy thereby stimulating excessive proinflammatory cytokine production

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