Regulation of Btg2/TIS21/PC3 expression via reactive oxygen species–protein kinase C–ΝFκΒ pathway under stress conditions

Imran, Muhammad; Lim, In Kyoung

doi:10.1016/j.cellsig.2013.07.015

Cited by 45 publications

(34 citation statements)

References 63 publications

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“…Interestingly, some up-regulated lincRNAs occurred next to established stress response genes such as Btg2, Egr3, Ier2 and Ier3 (Fig. S1I) (Arlt and Schäfer, 2011;GallitanoMendel et al, 2008;Imran and Lim, 2013;Landau et al, 2012).…”

Section: Uv-induced Gene Expression Changes Primarily Occur At Expresmentioning

confidence: 99%

Dynamics of chromatin accessibility and epigenetic state in response to UV damage

Schick

Fournier

Thakurela

et al. 2015

Journal of Cell Science

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Epigenetic mechanisms determine the access of regulatory factors to DNA during events such as transcription and the DNA damage response. However, the global response of histone modifications and chromatin accessibility to UV exposure remains poorly understood. Here, we report that UV exposure results in a genome-wide reduction in chromatin accessibility, while the distribution of the active regulatory mark H3K27ac undergoes massive reorganization. Genomic loci subjected to epigenetic reprogramming upon UV exposure represent target sites for sequence-specific transcription factors. Most of these are distal regulatory regions, highlighting their importance in the cellular response to UV exposure. Furthermore, UV exposure results in an extensive reorganization of super-enhancers, accompanied by expression changes of associated genes, which may in part contribute to the stress response. Taken together, our study provides the first comprehensive resource for genome-wide chromatin changes upon UV irradiation in relation to gene expression and elucidates new aspects of this relationship.

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Section: Uv-induced Gene Expression Changes Primarily Occur At Expresmentioning

confidence: 99%

Dynamics of chromatin accessibility and epigenetic state in response to UV damage

Schick

Fournier

Thakurela

et al. 2015

Journal of Cell Science

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“…NF-κB activation has been known as an important event for macrophage differentiation [15][16][17], and serum deprivation activates NF-κB pathway through ROS generation [26]. We, therefore, evaluated the effect of ATRA treatment on NF-κB activation in HL-60 cells.…”

Section: Atra Treatment With Serum Deprivation Enhances Nf-κb Activatmentioning

confidence: 99%

“…We have previously reported that serum deprivation-induced ROS generation activates NF-κB [26], thus to investigate upstream signals of the serum deprivation-induced ROS-NF-κΒ cascade in macrophage differentiation, HL-60 cells were pretreated with MAPK kinase inhibitors including U0126 (MEK1/2 inhibitor), SP600125 (JNK inhibitor) and SB203580 (p38 MAPK inhibitor), and then exposed to serum deprivation for 1 h. NF-κB activation and its target gene, Btg2, transcription were assessed by immunoblot and RT-PCR analyses, respectively. Serum deprivation led to NF-κB activation as assessed by IΚΚα/β phosphorylation and IκΒα degradation.…”

Section: Serum Deprivation-induced Nf-κb Activation Is Regulated By Rmentioning

confidence: 99%

“…Previously we have reported stress-induced NF-κΒ activation in various cell lines [26]. Therefore, to assess the role of NF-κΒ in ATRAinduced differentiation, HL-60 cells were treated with ATRA (0.1 μM) or TPA (30 nM) in complete or serum deprived media, and changes of cell morphology, extent of cell adherence, surface markers of both granulocytes and macrophages, and differentiation specific gene expressions were analyzed (Fig.…”

Section: Atra Induces Macrophage-like Differentiation Of Hl-60 Cells mentioning

confidence: 99%

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Stress-induced NF-κB activation differentiates promyelocytic leukemia cells to macrophages in response to all-trans-retinoic acid

Imran

Park

Lim

2015

Cellular Signalling

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“…As illustrated in Figure 3C, treatment with BIO-11006 provoked a significant decrease in mRNA expression of these cytokines in the lung, suggesting effects at the message level. MARCKS also has been shown to be involved in activation of NF-kB in different cells (19)(20)(21), perhaps through a protein kinase C d-related mechanism (22), and it is known that KC and TNF-a-contain NF-kB-binding sites in their promoter regions, so a logical next step was to look at whether or not BIO-11006 could affect NF-kB. Using phosphorylation of the p65 subunit of NF-kB in lung cytoplasmic extracts as an indicator of NF-kB activation, inhalation of BIO-11006 at any of the time points in this study inhibited LPS-induced NF-kB activation (Figure 4).…”

Section: Actin-binding Function Of Marcks (4)mentioning

confidence: 99%

An Inhaled Inhibitor of Myristoylated Alanine-Rich C Kinase Substrate Reverses LPS-Induced Acute Lung Injury in Mice

Yin

Fang

Park³

et al. 2016

Am J Respir Cell Mol Biol

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Intratracheal instillation of bacterial LPS is a well-established model of acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS). Because the myristoylated alanine-rich C kinase substrate (MARCKS) protein is involved in neutrophil migration and proinflammatory cytokine production, we examined whether an aerosolized peptide that inhibits MARCKS function could attenuate LPS-induced lung injury in mice. The peptide, BIO-11006, was delivered at 50 mM via inhalation either just before intratracheal instillation of 5 mg of LPS into Balb/C mice, or 4, 12, 24, or 36 hours after LPS instillation. Effects of BIO-11006 were evaluated via analysis of mouse disease-related behavior, lung histology, bronchoalveolar lavage fluid total protein, neutrophil counts and percentages, cytokine (KC [CXCl1, mouse IL-8 equivalent] and TNF-a) expression, and activation of NF-kB in lung tissue. Treatment with aerosolized BIO-11006 at 0, 4, 12, 24, and even 36 hours after LPS instillation reversed the disease process: mouse behavior returned to normal after two treatments 12 hours apart with the inhaled peptide after LPS injury, whereas control LPS-instilled animals treated with PBS only remained moribund. Histological appearance of inflammation, bronchoalveolar lavage fluid protein levels, leukocyte and neutrophil numbers, KC and TNF-a gene and protein expression, and NF-kB activation were all significantly attenuated by inhaled BIO-11006 at all time points. These results implicate MARCKS protein in the pathogenesis of ALI/ARDS and suggest that MARCKS-inhibitory peptide(s), delivered by inhalation, could represent a new and potent therapeutic treatment for ALI/ARDS, even if administered well after the disease process has begun.Keywords: myristoylated alanine-rich C kinase substrate; acute lung injury; LPS; neutrophils Clinical RelevanceThese studies show that treatment of mice with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) with an inhaled inhibitor of myristoylated alanine-rich C kinase substrate (MARCKS) protein reverses disease progression, even when treatment is initiated well into the disease process, a time when the animals are moribund. These results implicate MARCKS protein in the pathogenesis of ALI/ARDS and suggest that MARCKS-inhibitory peptide(s), delivered by inhalation, could represent a new and potent therapeutic treatment for ALI/ARDS, even if administered well after the disease process has begun. Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS), are major causes of respiratory failure; worldwide, over 1 million cases occur annually, with over 200,000 adult and 20,000 pediatric cases per year in the United States. This disorder is characterized by a large influx of leukocytes, especially neutrophils, to the lung as part of an acute inflammatory response, with injury to epithelial and endothelial cell barriers and pulmonary edema, all of which lead to respiratory failure. Treatment options remain limited to mechanical ventilation...

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Regulation of Btg2/TIS21/PC3 expression via reactive oxygen species–protein kinase C–ΝFκΒ pathway under stress conditions

Cited by 45 publications

References 63 publications

Dynamics of chromatin accessibility and epigenetic state in response to UV damage

Dynamics of chromatin accessibility and epigenetic state in response to UV damage

Stress-induced NF-κB activation differentiates promyelocytic leukemia cells to macrophages in response to all-trans-retinoic acid

An Inhaled Inhibitor of Myristoylated Alanine-Rich C Kinase Substrate Reverses LPS-Induced Acute Lung Injury in Mice

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