Inhibition by Deacetylase Inhibitors of IL-1-Dependent Induction of Haptoglobin Involves CCAAT/Enhancer-Binding Protein Isoforms in Intestinal Epithelial Cells

2000 ◽  
Vol 276 (2) ◽  
pp. 673-679 ◽  
Author(s):  
Antoine Désilets ◽  
Ionela Gheorghiu ◽  
Shun-Jiang Yu ◽  
Ernest G. Seidman ◽  
Claude Asselin
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Binding Protein ◽  
Protein Isoforms ◽  
Intestinal Epithelial ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

scholarly journals Role of Specific CCAAT/Enhancer-binding Protein Isoforms in Intestinal Epithelial Cells

2001 ◽  
Vol 276 (47) ◽  
pp. 44331-44337 ◽  
Author(s):  
Ionela Gheorghiu ◽  
Claude Deschênes ◽  
Mylène Blais ◽  
François Boudreau ◽  
Nathalie Rivard ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Binding Protein ◽  
Protein Isoforms ◽  
Intestinal Epithelial ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

scholarly journals JunD Represses Transcription and Translation of the Tight Junction Protein Zona Occludens-1 Modulating Intestinal Epithelial Barrier Function

2008 ◽  
Vol 19 (9) ◽  
pp. 3701-3712 ◽  
Author(s):  
Jie Chen ◽  
Lan Xiao ◽  
Jaladanki N. Rao ◽  
Tongtong Zou ◽  
Lan Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junction ◽  
Barrier Function ◽  
Intestinal Epithelial Cells ◽  
Binding Protein ◽  
Mrna Translation ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function

The AP-1 transcription factor JunD is highly expressed in intestinal epithelial cells, but its exact role in maintaining the integrity of intestinal epithelial barrier remains unknown. The tight junction (TJ) protein zonula occludens (ZO)-1 links the intracellular domain of TJ-transmembrane proteins occludin, claudins, and junctional adhesion molecules to many cytoplasmic proteins and the actin cytoskeleton and is crucial for assembly of the TJ complex. Here, we show that JunD negatively regulates expression of ZO-1 and is implicated in the regulation of intestinal epithelial barrier function. Increased JunD levels by ectopic overexpression of the junD gene or by depleting cellular polyamines repressed ZO-1 expression and increased epithelial paracellular permeability. JunD regulated ZO-1 expression at the levels of transcription and translation. Transcriptional repression of ZO-1 by JunD was mediated through cAMP response element-binding protein-binding site within its proximal region of the ZO-1-promoter, whereas induced JunD inhibited ZO-1 mRNA translation by enhancing the interaction of the ZO-1 3′-untranslated region with RNA-binding protein T cell-restricted intracellular antigen 1-related protein. These results indicate that JunD is a biological suppressor of ZO-1 expression in intestinal epithelial cells and plays a critical role in maintaining epithelial barrier function.

scholarly journals Transcriptional regulation of importin-α1 by JunD modulates subcellular localization of RNA-binding protein HuR in intestinal epithelial cells

2016 ◽  
Vol 311 (6) ◽  
pp. C874-C883 ◽  
Author(s):  
Yan Xu ◽  
Jie Chen ◽  
Lan Xiao ◽  
Hee Kyoung Chung ◽  
Yuan Zhang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Subcellular Localization ◽  
Rna Binding ◽  
Nuclear Translocation ◽  
Intestinal Epithelial Cells ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Intestinal Epithelial ◽  
Mucosal Regeneration ◽  
Importin Α

The RNA-binding protein HuR is crucial for normal intestinal mucosal regeneration by modulating the stability and translation of target mRNAs, but the exact mechanism underlying HuR trafficking between the cytoplasm and nucleus remains largely unknown. Here we report a novel function of transcription factor JunD in the regulation of HuR subcellular localization through the control of importin-α1 expression in intestinal epithelial cells (IECs). Ectopically expressed JunD specifically inhibited importin-α1 at the transcription level, and this repression is mediated via interaction with CREB-binding site that was located at the proximal region of importin-α1 promoter. Reduction in the levels of importin-α1 by JunD increased cytoplasmic levels of HuR, although it failed to alter whole cell HuR levels. Increased levels of endogenous JunD by depleting cellular polyamines also inhibited importin-α1 expression and increased cytoplasmic HuR levels, whereas JunD silencing rescued importin-α1 expression and enhanced HuR nuclear translocation in polyamine-deficient cells. Moreover, importin-α1 silencing protected IECs against apoptosis, which was prevented by HuR silencing. These results indicate that JunD regulates HuR subcellular distribution by downregulating importin-α1, thus contributing to the maintenance of gut epithelium homeostasis.

scholarly journals miR-222 represses expression of zipcode binding protein-1 and phospholipase C-γ1 in intestinal epithelial cells

2019 ◽  
Vol 316 (3) ◽  
pp. C415-C423 ◽  
Author(s):  
Li-Ping Jiang ◽  
Shelley R. Wang ◽  
Hee Kyoung Chung ◽  
Saharsh Buddula ◽  
Jian-Ying Wang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cells ◽  
Phospholipase C ◽  
Intestinal Epithelial Cells ◽  
Binding Protein ◽  
Acute Injury ◽  
Intestinal Epithelial ◽  
Small Interfering Rnas ◽  
The Stability ◽  
Wounded Area

Both zipcode binding protein-1 (ZBP1) and phospholipase C-γ1 (PLCγ1) are intimately involved in many aspects of early intestinal mucosal repair after acute injury, but the exact mechanisms that control their cellular abundances remain largely unknown. The present study shows that microRNA-222 (miR-222) interacts with the mRNAs encoding ZBP1 and PLCγ1 and regulates ZBP1 and PLCγ1 expression in intestinal epithelial cells (IECs). The biotinylated miR-222 bound specifically to the ZBP1 and PLCγ1 mRNAs in IECs. Ectopically expressed miR-222 precursor destabilized the ZBP1 and PLCγ1 mRNAs and consequently lowered the levels of cellular ZBP1 and PLCγ1 proteins. Conversely, decreasing the levels of cellular miR-222 by transfection with its antagonism increased the stability of the ZBP1 and PLCγ1 mRNAs and increased the levels of ZBP1 and PLCγ1 proteins. Overexpression of miR-222 also inhibited cell migration over the wounded area, which was partially abolished by overexpressing ZBP1 and PLCγ1. Furthermore, prevention of the increased levels of ZBP1 and PLCγ1 in the miR-222-silenced cells by transfection with specific small interfering RNAs targeting ZBP1 or PLCγ1 mRNA inhibited cell migration after wounding. These findings indicate that induced miR-222 represses expression of ZBP1 and PLCγ1 at the posttranscriptional level, thus inhibiting IEC migration during intestinal epithelial restitution after wounding.

DIFFERENTIAL REGULATION OF MACROPHAGE CCAAT-ENHANCER BINDING PROTEIN ISOFORMS BY LIPOPOLYSACCHARIDE AND CYTOKINES

Cytokine ◽  
2000 ◽  
Vol 12 (9) ◽  
pp. 1430-1436 ◽  
Author(s):  
Tengku S Tengku-Muhammad ◽  
Timothy R Hughes ◽  
Harri Ranki ◽  
Anthony Cryer ◽  
Dipak P Ramji
Keyword(s):  
Binding Protein ◽  
Differential Regulation ◽  
Protein Isoforms ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein
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