Endoplasmic Reticulum Stress-activated C/EBP Homologous Protein Enhances Nuclear Factor-κB Signals via Repression of Peroxisome Proliferator-activated Receptor γ

Park, Seonghwan; Choi, Hye Jin; Yang, Hyun; Hun, Kee; Kim, Juil; Lee, Jun Young; Moon, Yuseok

doi:10.1074/jbc.m110.136259

Cited by 79 publications

(72 citation statements)

References 57 publications

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“…This negative relationship during the ER stress was proven in our recent report that ER stress-induced CHOP suppresses PPAR␥ expression (28). In the present study, suppression of CHOP using CHOP shRNA expression enhanced PPAR␥ expression in response to chemical ER stress TG, indicating regulatory action of CHOP on PPAR␥ levels (Fig.…”

Section: Chop Modulates In-and-out Behavior Of Hur Protein By Limitinsupporting

confidence: 60%

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Two In-and-out Modulation Strategies for Endoplasmic Reticulum Stress-linked Gene Expression of Pro-apoptotic Macrophage-inhibitory Cytokine 1

Park

Choi

Yang

et al. 2012

Journal of Biological Chemistry

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Background: Modulation of a pro-apoptotic MIC-1 was addressed under ER stress-linked alterations of intracellular components. Results: Transporting of transcript-associated complex across cellular compartments is critical for MIC-1 mRNA stabilization. Conclusion: Stabilization is due to complex formation with pumped-out RNA-binding protein and their timely exit from the stress granule. Significance: Harmonized in-and-out modulation implicates key regulatory processes of MIC-1 expression in ER stress-linked therapy and biology.

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Section: Chop Modulates In-and-out Behavior Of Hur Protein By Limitinsupporting

confidence: 60%

“…ER stressinduced CHOP is basically a negative modulator of PPAR␥ expression. Our previous investigation suggests that CHOP protein interferes with the homodimeric C/EBP␤, which is a critical transcriptional activator of PPAR␥ induction (28). Otherwise, enhanced PPAR␥ bound to and detained the active form of PKC␣ in the cytoplasm.…”

Section: Discussionmentioning

confidence: 99%

Two In-and-out Modulation Strategies for Endoplasmic Reticulum Stress-linked Gene Expression of Pro-apoptotic Macrophage-inhibitory Cytokine 1

Park

Choi

Yang

et al. 2012

Journal of Biological Chemistry

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“…A number of studies have identified cross-talk mechanisms between the UPR and proinflammatory pathways, including NF-kB signaling (20)(21)(22). Consequently, the goal of this study was to investigate how the UPR and ER stress might contribute to the damaging hyper-inflammatory phenotype in CF.…”

mentioning

confidence: 99%

Atypical Activation of the Unfolded Protein Response in Cystic Fibrosis Airway Cells Contributes to p38 MAPK-Mediated Innate Immune Responses

Blohmke

Mayer

Tang

et al. 2012

The Journal of Immunology

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Inflammatory lung disease is the major cause of morbidity and mortality in cystic fibrosis (CF); understanding what produces dysregulated innate immune responses in CF cells will be pivotal in guiding the development of novel anti-inflammatory therapies. To elucidate the molecular mechanisms that mediate exaggerated inflammation in CF following TLR signaling, we profiled global gene expression in immortalized human CF and non-CF airway cells at baseline and after microbial stimulation. Using complementary analysis methods, we observed a signature of increased stress levels in CF cells, specifically characterized by endoplasmic reticulum (ER) stress, the unfolded protein response (UPR), and MAPK signaling. Analysis of ER stress responses revealed an atypical induction of the UPR, characterized by the lack of induction of the PERK–eIF2α pathway in three complementary model systems: immortalized CF airway cells, fresh CF blood cells, and CF lung tissue. This atypical pattern of UPR activation was associated with the hyperinflammatory phenotype in CF cells, as deliberate induction of the PERK–eIF2α pathway with salubrinal attenuated the inflammatory response to both flagellin and Pseudomonas aeruginosa. IL-6 production triggered by ER stress and microbial stimulation were both dependent on p38 MAPK activity, suggesting a molecular link between both signaling events. These data indicate that atypical UPR activation fails to resolve the ER stress in CF and sensitizes the innate immune system to respond more vigorously to microbial challenge. Strategies to restore ER homeostasis and normalize the UPR activation profile may represent a novel therapeutic approach to minimize lung-damaging inflammation in CF.

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“…Apoptosis of HPMCs using a higher concentration of ER stress inducers was associated with a persistent increase in the expression of C/EBP homologous protein (CHOP; Figure 6a), a UPR marker has been implicated in apoptosis. 19,37,38 A mild and transient upregulation of CHOP was observed with a lower concentration of TM or TG (Figure 6b).…”

Section: Er Stress Induces Snail Expression and Nuclearmentioning

confidence: 99%

Endoplasmic reticulum stress as a novel target to ameliorate epithelial-to-mesenchymal transition and apoptosis of human peritoneal mesothelial cells

Shin

Ryu

et al. 2015

Laboratory Investigation

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Endoplasmic Reticulum Stress-activated C/EBP Homologous Protein Enhances Nuclear Factor-κB Signals via Repression of Peroxisome Proliferator-activated Receptor γ

Cited by 79 publications

References 57 publications

Two In-and-out Modulation Strategies for Endoplasmic Reticulum Stress-linked Gene Expression of Pro-apoptotic Macrophage-inhibitory Cytokine 1

Two In-and-out Modulation Strategies for Endoplasmic Reticulum Stress-linked Gene Expression of Pro-apoptotic Macrophage-inhibitory Cytokine 1

Atypical Activation of the Unfolded Protein Response in Cystic Fibrosis Airway Cells Contributes to p38 MAPK-Mediated Innate Immune Responses

Endoplasmic reticulum stress as a novel target to ameliorate epithelial-to-mesenchymal transition and apoptosis of human peritoneal mesothelial cells

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