Involvement of phospholipase C in Yersinia enterocolitica heat stable enterotoxin (Y-STa) mediated rise in intracellular calcium level in rat intestinal epithelial cells

Toxicon ◽  
2005 ◽  
Vol 45 (3) ◽  
pp. 361-367 ◽  
Author(s):  
Subhrajit Saha ◽  
Dyuti Dutta Gupta ◽  
Manoj K. Chakrabarti
Keyword(s):  
Epithelial Cells ◽  
Intracellular Calcium ◽  
Phospholipase C ◽  
Yersinia Enterocolitica ◽  
Calcium Level ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Heat Stable ◽  
Intracellular Calcium Level

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.

scholarly journals Simultaneous Exposure to Escherichia coli Heat-Labile and Heat-Stable Enterotoxins Increases Fluid Secretion and Alters Cyclic Nucleotide and Cytokine Production by Intestinal Epithelial Cells

2014 ◽  
Vol 82 (12) ◽  
pp. 5308-5316 ◽  
Author(s):  
Lisa T. Read ◽  
Rachel W. Hahn ◽  
Carli C. Thompson ◽  
David L. Bauer ◽  
Elizabeth B. Norton ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Diarrheal Disease ◽  
Water Movement ◽  
Intestinal Epithelial Cells ◽  
Intestinal Lumen ◽  
Intestinal Epithelial ◽  
Simultaneous Exposure ◽  
Heat Stable ◽  
Heat Labile

ABSTRACTEnterotoxigenicEscherichia coli(ETEC) is a significant cause of diarrheal disease and death, especially in children in developing countries. ETEC causes disease by colonizing the small intestine and producing heat-labile toxin (LT), heat-stable toxin (ST), or both LT and ST (LT+ST). The majority of ETEC strains produce both ST and LT. Despite the prevalence of LT+ST-producing organisms, few studies have examined the physiologic or immunologic consequences of simultaneous exposure to these two potent enterotoxins. In the current report, we demonstrate that when LT and ST are both present, they increase water movement into the intestinal lumen over and above the levels observed with either toxin alone. As expected, cultured intestinal epithelial cells increased their expression of intracellular cyclic GMP (cGMP) when treated with ST and their expression of intracellular cyclic AMP (cAMP) when treated with LT. When both toxins were present, cGMP levels but not cAMP levels were synergistically elevated compared with the levels of expression caused by the corresponding single-toxin treatment. Our data also demonstrate that the levels of inflammatory cytokines produced by intestinal epithelial cells in response to LT are significantly reduced in animals exposed to both enterotoxins. These findings suggest that there may be complex differences between the epithelial cell intoxication and, potentially, secretory outcomes induced by ETEC strains expressing LT+ST compared with strains that express LT or ST only. Our results also reveal a novel mechanism wherein ST production may reduce the hosts' ability to mount an effective innate or adaptive immune response to infecting organisms.

scholarly journals Leukotriene D4 induces association of active RhoA with phospholipase C-γ1 in intestinal epithelial cells

2002 ◽  
Vol 365 (1) ◽  
pp. 157-163 ◽  
Author(s):  
Charles Kumar THODETI ◽  
Ramin MASSOUMI ◽  
Lene BINDSLEV ◽  
Anita SJÖLANDER
Keyword(s):  
Plasma Membrane ◽  
Epithelial Cells ◽  
Phospholipase C ◽  
Fluorescent Protein ◽  
Intestinal Epithelial Cells ◽  
Dependent Manner ◽  
Intestinal Epithelial ◽  
Leukotriene D4 ◽  
Green Fluorescent ◽  
Constitutively Active

It has been previously suggested that leukotriene-induced Ca2+ signalling is mediated through a Rho-dependent process, but neither direct activation of Rho nor a mechanism underlying such signalling has been reported. Accordingly, we used the Rhotekin binding assay to assess RhoA activation in intestinal epithelial cells and observed that RhoA was activated by leukotriene D4 (LTD4). We also found that, within 15s, activation of RhoA by LTD4 led to an increased association of RhoA with G-protein βγ (Gβγ) and phospholipase C-γ1 (PLC-γ1) in the plasma membrane, as evidenced by the results of co-immunoprecipitation, glutathione S-transferase (GST) pulldown assays, and confocal microscopy. Amounts of RhoA increased in both Gβ and PLC-γ1 immunoprecipitates within 15s of LTD4 treatment. An interaction between RhoA, Gβγ and PLC-γ1 is supported by our finding that a GST fusion protein of constitutively active RhoA (GST-RhoAV14) precipitated Gβγ and PLC-γ1 from cell lysates in an agonist-dependent manner. Such an association is also substantiated by our confocal immunofluorescence results, which revealed that LTD4 induction increased co-localization of constitutively active RhoA and PLC-γ1 to the plasma membrane of cells transfected with enhanced green fluorescent protein L63RhoA. Furthermore, microinjection of neutralizing RhoA antibodies, but not control antibodies, significantly reduced LTD4-induced Ca2+ mobilization. Our results are the first to demonstrate a LTD4-induced activation of RhoA and more importantly its association with PLC-γ1, which are essential for the PLC-γ1-mediated calcium mobilization.

scholarly journals Escherichia coli Heat-Stable Enterotoxin Mediates Na+/H+ Exchanger 4 Inhibition Involving cAMP in T84 Human Intestinal Epithelial Cells

PLoS ONE ◽  
2015 ◽  
Vol 10 (12) ◽  
pp. e0146042 ◽  
Author(s):  
Ana R. Beltrán ◽  
Luciene R. Carraro-Lacroix ◽  
Camila N. A. Bezerra ◽  
Marcelo Cornejo ◽  
Katrina Norambuena ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Heat Stable ◽  
Human Intestinal Epithelial Cells
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