The acetyltransferase HAT1 moderates the NF-κB response by regulating the transcription factor PLZF

Sadler, Anthony John; Suliman, Bandar Ali; Yu, Liang; Yuan, Xiangliang; Wang, Die; Irving, Aaron T.; Sarvestani, Soroush T.; Banerjee, Aditi; Mansell, Ashley; Liu, Junping; Gerondakis, Steven Demetrious; Williams, Bryan R.G.; Xu, Dakang

doi:10.1038/ncomms7795

Cited by 68 publications

(73 citation statements)

References 27 publications

(25 reference statements)

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“…This protein forms a repressor complex that inhibits NFKB signaling. 22 In addition, miR-140 downregulated a number of other proteins involved in the NFKB pathway. ANXA6 is increased in human OA cartilage.…”

Section: Discussionmentioning

confidence: 99%

microRNA-140 Inhibits Inflammation and Stimulates Chondrogenesis in a Model of Interleukin 1β-induced Osteoarthritis

Karlsen

Souza

Ødegaard

et al. 2016

Molecular Therapy - Nucleic Acids

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Osteoarthritis is a serious disease of articular cartilage. The pathogenic factors contributing to this disorder are inflammation, extracellular matrix degradation and failure to rebuild the articular cartilage. Preclinical studies suggest that microRNA-140 may play a protective role in osteoarthritis development, but little is known about the mechanism by which this occurs. Here we present the results of forced expression of microRNA-140 in an in vitro model of osteoarthritis, evaluated by global proteomics analysis. We show that inflammation was reduced through the altered levels of multiple proteins involved in the nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 pathway. microRNA-140 upregulated many of the components involved in the synthesis of hyaline extracellular matrix and reduced the levels of aggrecanases and syndecan 4, thus potentially both increasing cartilage repair and reducing cartilage breakdown. These results show how forced expression of microRNA-140 is likely to counteract all three pathogenic processes, and support the idea that intra-articular injection of microRNA-140 may benefit patients suffering from early osteoarthritis.

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Section: Discussionmentioning

confidence: 99%

microRNA-140 Inhibits Inflammation and Stimulates Chondrogenesis in a Model of Interleukin 1β-induced Osteoarthritis

Karlsen

Souza

Ødegaard

et al. 2016

Molecular Therapy - Nucleic Acids

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“…Although this transcriptional repressor is predominantly involved in cell cycle and differentiation processes in different types of cells (47), the potential roles of PLZF in the airway epithelium are not well understood. PLZF has been reported to mediate GC antiproliferative and apoptotic actions in lymphocytes (24,48) and to modulate inflammatory responses to pathogens through repression of NF-kB pathways in bone marrow-derived macrophages (49). Limiting induction of PLZF by ICS may therefore impair their anti-inflammatory effects, Figure 5.…”

Section: Discussionmentioning

confidence: 99%

Cortisol limits selected actions of synthetic glucocorticoids in the airway epithelium

et al. 2018

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Cortisol, a physiologic glucocorticoid (GC), is essential for growth and differentiation of the airway epithelium. Epithelial function influences inflammation in chronic respiratory diseases. Synthetic GCs, including inhaled corticosteroids, exert anti-inflammatory effects in airway epithelium by transactivation of genes and by inhibition of proinflammatory cytokine release. We examined the effect of cortisol on the actions of synthetic GCs in the airway epithelium, demonstrating that cortisol acts like a partial agonist at the GC receptor (GR), limiting GCinduced GR-dependent transcription in the BEAS-2B human bronchial epithelial cell line. Cortisol also limited the inhibition of granulocyte macrophage colony-stimulating factor release by synthetic GCs in TNF-a-activated BEAS-2B cells. The relevance of these findings is supported by observations on tracheal epithelium obtained from mice treated for 5 d with systemic GC, showing limitations in selected GC effects, including inhibition of IL-6. Moreover, gene transactivation by synthetic GCs was compromised by standard air-liquid interface (ALI) growth medium cortisol concentration (1.4 mM) in the ALI-differentiated organotypic culture of primary human airway epithelial cells. These findings suggest that endogenous corticosteroids may limit certain actions of synthetic pharmacological GCs and contribute to GC insensitivity, particularly when corticosteroid levels are elevated by

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“…A role of ZBTB16 in the control of inflammation is emerging. ZBTB16 would form a co-repressor complex with HDAC3 and NF-κB in order to moderate the inflammatory program [51, 52]. A possible function of ZBTB16 in placenta physiopathology remains to be explored, however a recent study linked it to hydatidiform molar pregnancies through its physical interaction with NLRP7 [53].…”

Section: Discussionmentioning

confidence: 99%

An Integrative Analysis of Preeclampsia Based on the Construction of an Extended Composite Network Featuring Protein-Protein Physical Interactions and Transcriptional Relationships

Vaiman

Miralles

2016

PLoS ONE

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Preeclampsia (PE) is a pregnancy disorder defined by hypertension and proteinuria. This disease remains a major cause of maternal and fetal morbidity and mortality. Defective placentation is generally described as being at the root of the disease. The characterization of the transcriptome signature of the preeclamptic placenta has allowed to identify differentially expressed genes (DEGs). However, we still lack a detailed knowledge on how these DEGs impact the function of the placenta. The tools of network biology offer a methodology to explore complex diseases at a systems level. In this study we performed a cross-platform meta-analysis of seven publically available gene expression datasets comparing non-pathological and preeclamptic placentas. Using the rank product algorithm we identified a total of 369 DEGs consistently modified in PE. The DEGs were used as seeds to build both an extended physical protein-protein interactions network and a transcription factors regulatory network. Topological and clustering analysis was conducted to analyze the connectivity properties of the networks. Finally both networks were merged into a composite network which presents an integrated view of the regulatory pathways involved in preeclampsia and the crosstalk between them. This network is a useful tool to explore the relationship between the DEGs and enable hypothesis generation for functional experimentation.

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The acetyltransferase HAT1 moderates the NF-κB response by regulating the transcription factor PLZF

Cited by 68 publications

References 27 publications

microRNA-140 Inhibits Inflammation and Stimulates Chondrogenesis in a Model of Interleukin 1β-induced Osteoarthritis

microRNA-140 Inhibits Inflammation and Stimulates Chondrogenesis in a Model of Interleukin 1β-induced Osteoarthritis

Cortisol limits selected actions of synthetic glucocorticoids in the airway epithelium

An Integrative Analysis of Preeclampsia Based on the Construction of an Extended Composite Network Featuring Protein-Protein Physical Interactions and Transcriptional Relationships

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