Interferon Regulatory Factor-1 Regulates the Autophagic Response in LPS-Stimulated Macrophages through Nitric Oxide

Zhang, Lemeng; Cardinal, Jon; Bahar, Runalia; Evankovich, John; Huang, Hai; Nace, Gary W.; Billiar, Timothy R.; Rosengart, Matthew R.; Pan, Pinhua; Tsung, Allan

doi:10.2119/molmed.2011.00282

Cited by 37 publications

(32 citation statements)

References 66 publications

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“…In addition, the activation of the lymphotoxin-beta receptor induced expression of IRF-1, one of the major transcription factors of IL-8 gene [35]. Other data support evidence that IRF-1 activation is also necessary to inhibit autophagy [36]. …”

Section: Discussionmentioning

confidence: 95%

Porphyromonas gingivalis and its lipopolysaccharide differently modulate epidermal growth factor–dependent signaling in human gingival epithelial cells

Elkaïm

Bugueno

Benkirane‐Jessel

et al. 2017

Journal of Oral Microbiology

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Periodontitis is an inflammatory disease induced by pathogenic bacteria such as Porphyromonas gingivalis. Little is known about epidermal growth factor (EGF) signals in human gingival epithelial cells (HGEC), which are major targets of P. gingivalis, and how the expression of proteins participating in EGF signaling—that is, EGF-receptor (EGFR), suppressor of cytokine signaling-3 (SOCS-3), interferon regulatory factor-1 (IRF-1), and signal transducers and activators of transcription (STAT-3)—are modified. This study aimed to assess the effects of P. gingivalis and its purified lipopolysaccharide (LPS-Pg) on EGF signaling. HGEC were infected for 2 h in a dose-dependent manner with P. gingivalis and with heat-killed P. gingivalis, and activated for 2 and 24 h by 1 µg/mL of purified LPS-Pg. Quantitative reverse transcription polymerase chain reaction and Western blotting were performed to measure mRNA and protein levels for SOCS-3, IRF-1 EGF, EGFR, and STAT-3. The tyrosine-phosphorylation status of STAT-3 was also examined. The results showed that infection of HGEC cells with P. gingivalis, but not with heat-killed P. gingivalis, led to significant reductions in expression levels of mRNAs and proteins for SOCS-3, IRF-1, and EGFR, while LPS-Pg over time significantly increased the expression of these mRNAs and proteins. Tyrosine-phosphorylation of STAT-3 was significantly increased during infection with P. gingivalis and activation by LPS-Pg but not modified during infection with heat-killed P. gingivalis. This study highlights that P. gingivalis and its purified LPS differentially modulated the expression of proteins (SOCS-3, IRF-1, EGFR, and STAT-3) interfering with EGF signaling.

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Section: Discussionmentioning

confidence: 95%

Porphyromonas gingivalis and its lipopolysaccharide differently modulate epidermal growth factor–dependent signaling in human gingival epithelial cells

Elkaïm

Bugueno

Benkirane‐Jessel

et al. 2017

Journal of Oral Microbiology

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“…Furthermore, resveratrol inhibits LPS‐induced NO generation (Zong et al, ) and increases autophagic responses, suggesting that there may be a relationship between NO generation and autophagy. In this regard, it should be noted that NO inhibits macrophage autophagy during LPS stimulation (Zhang et al, ), and reduced NO generation may explain the increased autophagic response induced by resveratrol.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol inhibits NLRP3 inflammasome activation by preserving mitochondrial integrity and augmenting autophagy

et al. 2015

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The NLRP3 inflammasome is a caspase-1-containing multi-protein complex that controls the release of IL-1β and plays important roles in the development of inflammatory disease. Here, we report that resveratrol, a polyphenolic compound naturally produced by plants, inhibits NLRP3 inflammasome-derived IL-1β secretion and pyroptosis in macrophages. Resveratrol inhibits the activation step of the NLRP3 inflammasome by suppressing mitochondrial damage. Resveratrol also induces autophagy by activating p38, and macrophages treated with an autophagy inhibitor are resistant to the suppressive effects of resveratrol. In addition, resveratrol administration mitigates glomerular proliferation, glomerular sclerosis, and glomerular inflammation in a mouse model of progressive IgA nephropathy. These findings were associated with decreased renal mononuclear leukocyte infiltration, reduced renal superoxide anion levels, and inhibited renal NLRP3 inflammasome activation. Our data indicate that resveratrol suppresses NLRP3 inflammasome activation by preserving mitochondrial integrity and by augmenting autophagy.

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“…Interestingly, however, our findings indicate that IRF1 is an upstream regulator of STAT3 and AKT. Recently, the group of Zhang [32] demonstrated that overexpression of IRF1 increases mTOR phosphorylation in murine macrophages. Sarbassov et al [33] reported that knockdown of mTOR expression results in decreased p-AKT (Ser473 and Thr308) expression.…”

Section: Discussionmentioning

confidence: 99%

Repression of microRNA-130b by thyroid hormone enhances cell motility

Lin

Liao

et al. 2015

Journal of Hepatology

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Interferon Regulatory Factor-1 Regulates the Autophagic Response in LPS-Stimulated Macrophages through Nitric Oxide

Cited by 37 publications

References 66 publications

Porphyromonas gingivalis and its lipopolysaccharide differently modulate epidermal growth factor–dependent signaling in human gingival epithelial cells

Porphyromonas gingivalis and its lipopolysaccharide differently modulate epidermal growth factor–dependent signaling in human gingival epithelial cells

Resveratrol inhibits NLRP3 inflammasome activation by preserving mitochondrial integrity and augmenting autophagy

Repression of microRNA-130b by thyroid hormone enhances cell motility

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