CFTR protein expression in healthy men spermatozoa is not correlated with fertilization rate of ova

2010 ◽  
Vol 34 (8) ◽  
pp. S12-S12
Author(s):  
Hong‑Ge Li ◽  
Chen Min Xu ◽  
Kun Li ◽  
Ya Ni ◽  
Wen‑Ying Chen ◽  
...  
Keyword(s):  
Protein Expression ◽  
Fertilization Rate ◽  
Healthy Men ◽  
Cftr Protein

scholarly journals Impact of Heterogeneity within Cultured Cells on Bacterial Invasion: Analysis of Pseudomonas aeruginosa andSalmonella enterica Serovar Typhi Entry into MDCK cells by Using a Green Fluorescent Protein-Labelled Cystic Fibrosis Transmembrane Conductance Regulator Receptor

2000 ◽  
Vol 68 (2) ◽  
pp. 861-870 ◽  
Author(s):  
A. Alev Gerçeker ◽  
Tanweer Zaidi ◽  
Peter Marks ◽  
David E. Golan ◽  
Gerald B. Pier
Keyword(s):  
Epithelial Cells ◽  
Protein Expression ◽  
Fluorescent Protein ◽  
Cultured Cells ◽  
Mdck Cells ◽  
Transmembrane Conductance Regulator ◽  
Transmembrane Conductance ◽  
Bacterial Uptake ◽  
Cftr Protein ◽  
Green Fluorescent

ABSTRACT The cystic fibrosis transmembrane conductance regulator (CFTR) is a chloride ion channel that also serves as a receptor for entry ofPseudomonas aeruginosa and Salmonella entericaserovar Typhi into epithelial cells. To evaluate heterogeneity in CFTR protein expression in cultured cells and the effect of heterogeneity on internalization of different P. aeruginosa and serovar Typhi strains, we used two-color flow cytometry and confocal laser microscopy to study bacterial uptake by Madin-Darby canine kidney (MDCK) type I epithelial cells stably expressing a green fluorescent protein (GFP)-CFTR fusion construct (MDCK–GFP-CFTR cells). We found a strong correlation between cell size and GFP-CFTR protein expression, with 60 to 70% of cells expressing low levels of GFP-CFTR protein, 20 to 30% expressing intermediate levels, and <10% expressing high levels. The cells were sorted into low-, intermediate-, or high-level producers of CFTR protein; in vitro growth of each sorted population yielded the same distribution of CFTR protein expression as that in the original population. Cells expressing either low or high levels of CFTR protein internalized bacteria poorly; maximal bacterial uptake occurred in the cells expressing intermediate levels of CFTR protein. Treatment of MDCK cells with sodium butyrate markedly enhanced the production of CFTR protein without increasing cell size; butyrate treatment also increased the proportion of cells with internalized bacteria. However, there were fewer bacteria per butyrate-treated cell and, for P. aeruginosa, there was an overall decrease in the total level of bacterial uptake. The most highly ingested bacterial strains were internalized by fewer total MDCK–GFP-CFTR cells, indicating preferential bacterial uptake by a minority of epithelial cells within a given culture. Confocal fluorescence microscopy showed that P. aeruginosa and serovar Typhi induced cytoplasmic accumulation of CFTR protein close to the plasma membrane where the bacteria were adherent. These results show that within a population of MDCK–GFP-CFTR cells, there are cells with markedly different abilities to ingest bacteria via CFTR, the majority of the P. aeruginosa and serovar Typhi cells are ingested by the one-fourth to one-third of the cells that exhibit an intermediate size and level of CFTR protein expression, and overexpression of the CFTR receptor does not increase total bacterial uptake but rather allows more epithelial cells to ingest fewer total bacteria.

S1887 Dispersed Pancreatic Acini Have Strong CFTR Protein Expression and Exhibit An Anti-Apoptotic Phenotype in a Non-Acidic Extracellular Milieu

2008 ◽  
Vol 134 (4) ◽  
pp. A-287
Author(s):  
Kwang-Deok Moon ◽  
Stephen A. Ernst ◽  
Sae-Hong Lee ◽  
Chung Owyang ◽  
Matthew J. DiMagno
Keyword(s):  
Protein Expression ◽  
Pancreatic Acini ◽  
Extracellular Milieu ◽  
Cftr Protein

scholarly journals Contribution of CFTR to Alveolar Fluid Clearance by Lipoxin A4via PI3K/Akt Pathway in LPS-Induced Acute Lung Injury

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Yi Yang ◽  
Yang Cheng ◽  
Qing-Quan Lian ◽  
Li Yang ◽  
Wei Qi ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Protein Expression ◽  
Specific Inhibitor ◽  
Akt Pathway ◽  
Alveolar Type ◽  
Alveolar Fluid Clearance ◽  
Cftr Protein

The lipoxins are the first proresolution mediators to be recognized and described as the endogenous “braking signals” for inflammation. We evaluated the anti-inflammatory and proresolution bioactions of lipoxin A4in our lipopolysaccharide (LPS-)induced lung injury model. We demonstrated that lipoxin A4significantly improved histology of rat lungs and inhibited IL-6 and TNF-αin LPS-induced lung injury. In addition, lipoxin A4increased alveolar fluid clearance (AFC) and the effect of lipoxin A4on AFC was abolished byCFTRinh-172(a specific inhibitor of CFTR). Moreover, lipoxin A4could increase cystic fibrosis transmembrane conductance regulator (CFTR) protein expressionin vitroandin vivo. In rat primary alveolar type II (ATII) cells, LPS decreased CFTR protein expression via activation of PI3K/Akt, and lipoxin A4suppressed LPS-stimulated phosphorylation of Akt. These results showed that lipoxin A4enhanced CFTR protein expression and increased AFC via PI3K/Akt pathway. Thus, lipoxin A4may provide a potential therapeutic approach for acute lung injury.

scholarly journals ΔF508 CFTR protein expression in tissues from patients with cystic fibrosis

1999 ◽  
Vol 103 (10) ◽  
pp. 1379-1389 ◽  
Author(s):  
Nanette Kälin ◽  
Andreas Claaß ◽  
Martin Sommer ◽  
Edith Puchelle ◽  
Burkhard Tümmler
Keyword(s):  
Cystic Fibrosis ◽  
Protein Expression ◽  
Δf508 Cftr ◽  
Cftr Protein

scholarly journals Upregulation of CFTR Protects against Palmitate-Induced Endothelial Dysfunction by Enhancing Autophagic Flux

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Hongqi Chen ◽  
Wenliang Chen ◽  
Yinlian Yao ◽  
Naobei Ye ◽  
Ning Hou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Protein Expression ◽  
Cathepsin B ◽  
Cathepsin D ◽  
Ros Generation ◽  
Autophagic Flux ◽  
Protective Effects ◽  
Cftr Protein ◽  
Underlying Mechanisms

Saturated free fatty acids (FFAs) elevate in metabolic symptom leading to endothelial dysfunction. Cystic fibrosis transmembrane regulator (CFTR) functionally expresses in endothelial cells. The role of CFTR in FFA-induced endothelial dysfunction remains unclear. This study is aimed at exploring the effects of CFTR on palmitate- (PA-) induced endothelial dysfunction and its underlying mechanisms. We found that PA-induced endothelial dysfunction is characterized by a decrease of cell viability, reduction of NO generation and mitochondrial membrane potential, impairment of the tube formation, but an increase of ROS generation and cell apoptosis. Simultaneously, PA decreased CFTR protein expression. CFTR agonist Forskolin upregulated CFTR protein expression and protected against PA-induced endothelial dysfunction, while CFTR knockdown exacerbated endothelial dysfunction induced by PA and blunted the protective effects of Forskolin. In addition, PA impaired autophagic flux, and autophagic flux inhibitors aggravated PA-induced endothelial apoptosis. CFTR upregulation significantly restored autophagic flux in PA-insulted endothelial cells, which was involved in increasing the protein expression of Atg16L, Atg12-Atg5 complex, cathepsin B, and cathepsin D. In contrast, CFTR knockdown significantly inhibited the effects of Forskolin on autophagic flux and the expression of the autophagy-regulated proteins. Our findings illustrate that CFTR upregulation protects against PA-induced endothelial dysfunction by improving autophagic flux and underlying mechanisms are involved in enhancing autophagic signaling mediated by the Atg16L-Atg12-Atg5 complex, cathepsin B, and cathepsin D. CFTR might serve as a novel drug target for endothelial protection in cardiovascular diseases with a characteristic of elevation of FFAs.

Effects of ezetimibe and/or simvastatin on LDL receptor protein expression and on LDL receptor and HMG-CoA reductase gene expression: A randomized trial in healthy men

2008 ◽  
Vol 198 (1) ◽  
pp. 198-207 ◽  
Author(s):  
Ioanna Gouni-Berthold ◽  
Heiner K. Berthold ◽  
Helena Gylling ◽  
Maarit Hallikainen ◽  
Eleni Giannakidou ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Expression ◽  
Randomized Trial ◽  
Ldl Receptor ◽  
Receptor Protein ◽  
Hmg Coa Reductase ◽  
Healthy Men ◽  
Reductase Gene ◽  
Coa Reductase

Increased functional cell surface expression of CFTR and ΔF508-CFTR by the anthracycline doxorubicin

2001 ◽  
Vol 280 (5) ◽  
pp. C1031-C1037 ◽  
Author(s):  
Rangan Maitra ◽  
Collin M. Shaw ◽  
Bruce A. Stanton ◽  
Joshua W. Hamilton
Keyword(s):  
Cystic Fibrosis ◽  
Cell Surface ◽  
Protein Expression ◽  
Surface Expression ◽  
Chloride Secretion ◽  
Cell Surface Expression ◽  
Common Mutation ◽  
Transmembrane Conductance Regulator ◽  
Δf508 Cftr ◽  
Cftr Protein

Cystic fibrosis (CF) is a disease that is caused by mutations within the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The most common mutation, ΔF508, accounts for 70% of all CF alleles and results in a protein that is defective in folding and trafficking to the cell surface. However, ΔF508-CFTR is functional when properly localized. We report that a single, noncytotoxic dose of the anthracycline doxorubicin (Dox, 0.25 μM) significantly increased total cellular CFTR protein expression, cell surface CFTR protein expression, and CFTR-associated chloride secretion in cultured T84 epithelial cells. Dox treatment also increased ΔF508-CFTR cell surface expression and ΔF508-CFTR-associated chloride secretion in stably transfected Madin-Darby canine kidney cells. These results suggest that anthracycline analogs may be useful for the clinical treatment of CF.

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