Major Vault Protein Regulates Class A Scavenger Receptor-mediated Tumor Necrosis Factor-α Synthesis and Apoptosis in Macrophages

Ben, Jingjing; Zhang, Yan; Zhou, Rong‐Mei; Zhang, Haiyang; Zhu, Xudong; Li, Xiaoyü; Zhang, Hanwen; Li, Nan; Zhou, Xiaosi; Bai, Hui; Yang, Qing; Li, Donghai; Xu, Yong; Chen, Qi

doi:10.1074/jbc.m112.449538

Cited by 36 publications

(38 citation statements)

References 36 publications

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“…13 24 Caveolin-1 has been shown to be the binding partner of SR-A and plays an important role in regulating SR-A internalization. 14, 15 In this study, we found that low Cl − solution increased caveolin-1 expression both at baseline and after oxLDL treatment. Moreover, our results showed that reduction of [Cl − ]i enhances the formation of SR-A/caveolin-1 complex and triggers SR-A internalization.…”

Section: Discussionmentioning

confidence: 63%

“…14, 15 Indeed, SR-A colocalizes with caveolin-1 in the cell membrane ( Figure 4A). A co-immunoprecipitation Cl − movement across the cell plasma membrane has been suggested to play an important role in regulating a variety of physiological processes, including cell volume regulation, cell proliferation and apoptosis, inflammation, and synaptic transmission.…”

Section: Low CL − Solution Potentiates Caveolin-1-dependent Sr-a Intementioning

confidence: 99%

“…15 THP-1-derived macrophages were washed with PBS twice and scraped into 2 ml of lysis buffer (500 mmol/L Na2CO3, 1 mmol/L EDTA, 0.1% protease inhibitor cocktail, pH 11.0). Cell lysates were sonicated on ice with 3 times of 20-s bursts.…”

Section: Isolation Of Lipid Raftsmentioning

confidence: 99%

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Reduction of Intracellular Chloride Concentration Promotes Foam Cell Formation

Wu¹,

Liu²,

Xiong³

et al. 2016

Circ J

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Section: Discussionmentioning

confidence: 63%

Section: Low CL − Solution Potentiates Caveolin-1-dependent Sr-a Intementioning

confidence: 99%

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Reduction of Intracellular Chloride Concentration Promotes Foam Cell Formation

Wu¹,

Liu²,

Xiong³

et al. 2016

Circ J

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“…MVP/vaults have been associated with multidrug resistance (21)(22)(23), nuclear-cytoplasmic transport (24), innate immunity (25), autophagy (26), and signal transduction pathways (27)(28)(29)(30)(31); however, the precise function of MVP/ vault remains enigmatic. Our previous work indicating MVPinduced type I IFN production upon hepatitis C virus infection uncovers a new role of MVP in modulating innate immunity during viral infection (32).…”

mentioning

confidence: 99%

Inducible Major Vault Protein Plays a Pivotal Role in Double-Stranded RNA– or Virus-Induced Proinflammatory Response

Peng

Shi

Xia

et al. 2016

The Journal of Immunology

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Pathogen invasion triggers robust antiviral cytokine production via different transcription factor signaling pathways. We have previously demonstrated that major vault protein (MVP) induces type I IFN production during viral infection; however, little is known about the role of MVP in proinflammatory responses. In this study, we found in vitro that expression of MVP, IL-6, and IL-8 was inducible upon dsRNA stimulation or viral infection. Moreover, MVP was essential for the induction of IL-6 and IL-8, as impaired expression of IL-6 and IL-8 in MVP-deficient human PBMCs, human lung epithelial cells (A549), and THP-1 monocytes, as well as in murine splenocytes, peritoneal macrophages, and PBMCs from MVP-knockout (MVP−/−) mice, was observed. Upon investigation of the underlying mechanisms, we demonstrated that MVP acted in synergy with AP-1 (c-Fos) and CCAAT/enhancer binding protein (C/EBP)β–liver-enriched transcriptional activating protein to activate the IL6 and IL8 promoters. Introduction of mutations into the AP-1 and C/EBPβ binding sites on the IL6 and IL8 promoters resulted in the loss of synergistic activation with MVP. Furthermore, we found that MVP interacted with both c-Fos and C/EBPβ. The interactions promoted nuclear translocation and recruitment of these transcription factors to IL6 and IL8 promoter regions. In the MVP−/− mouse model, significantly decreased expression of early antiviral cytokines resulted in higher viral titer in the lung, higher mortality, and heavier lung damage after infection with lethal influenza A virus. Taken together, our findings help to delineate a novel role of MVP in host proinflammatory response.

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“…and are responsible for production of a wide spectrum of pro-inflammatory mediators (e.g. NO and tumor necrosis factor alpha, TNF␣) (Burke et al, 2003;Talks et al, 2000;Ben et al, 2013;Laskin et al, 2010;Fakhrzadeh, 2008;Parameswaran and Patial, 2010). Importantly, when recruited to tissue sites of infection or inflammation, macrophages immediately encounter a decreasing oxygen gradient, which leads to stabilization of hypoxia inducible factor-1 alpha (HIF-1␣) protein.…”

mentioning

confidence: 98%