scholarly journals Aldosterone Stimulates Activity and Surface Expression of NHE3 in Human Primary Proximal Tubule Epithelial Cells (RPTEC)

2006 ◽  
Vol 17 (1-2) ◽  
pp. 21-28 ◽  
Author(s):  
Karina Drumm ◽  
Theresia R. Kress ◽  
Birgit Gassner ◽  
Alexander W. Krug ◽  
Michael Gekle
Keyword(s):  
Epithelial Cells ◽  
Proximal Tubule ◽  
Surface Expression

scholarly journals GP96 drives exacerbation of secondary bacterial pneumonia following influenza A virus infection

2020 ◽  
Author(s):  
Tomoko Sumitomo ◽  
Masanobu Nakata ◽  
Satoshi Nagase ◽  
Yuki Takahara ◽  
Mariko Honda-Ogawa ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Influenza A Virus ◽  
Transcriptional Repression ◽  
Bacterial Pneumonia ◽  
Influenza A ◽  
Surface Expression ◽  
Lung Pathology ◽  
Direct Binding ◽  
Novel Therapeutic Strategies ◽  
Secondary Bacterial Pneumonia

AbstractInfluenza A virus (IAV) infection predisposes the host to secondary bacterial pneumonia, known as a major cause of morbidity and mortality during influenza epidemics. Analysis of interactions between IAV-infected human epithelial cells and Streptococcus pneumoniae revealed that infected cells ectopically exhibited the endoplasmic reticulum chaperon GP96 on the surface. Importantly, efficient pneumococcal adherence to epithelial cells was imparted by interactions with extracellular GP96 and integrin αV, with the surface expression mediated by GP96 chaperone activity. Furthermore, abrogation of adherence was gained by chemical inhibition or genetic knockout of GP96, as well as addition of RGD peptide. Direct binding of extracellular GP96 and pneumococci was shown to be mediated by pneumococcal oligopeptide permease components. Additionally, IAV infection induced activation of calpains and Snail1, which are responsible for degradation and transcriptional repression of junctional proteins in the host, respectively, indicating increased bacterial translocation across the epithelial barrier. Notably, treatment of IAV-infected mice with the GP96 inhibitor enhanced pneumococcal clearance from lung tissues and ameliorated lung pathology. Taken together, the present findings indicate a viral-bacterial synergy in relation to disease progression and suggest a paradigm for developing novel therapeutic strategies tailored to inhibit pneumococcal colonization in an IAV-infected respiratory tract.

QS394. The Genomic Analysis of the Heterogeneity Hypoxia Responses in Renal Proximal Tubule Epithelial Cells After Knock-Down of HIF-1α and HIF-2α

2008 ◽  
Vol 144 (2) ◽  
pp. 424
Author(s):  
Zhen Wang ◽  
Edwin H. Rodriguez ◽  
Michael T. Longaker ◽  
Patrick O. Brown ◽  
Jen-Tsan A. Chi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Proximal Tubule ◽  
Genomic Analysis ◽  
Renal Proximal Tubule ◽  
Knock Down

scholarly journals Bioinformatics analysis of proteomics profiles in senescent human primary proximal tubule epithelial cells

2016 ◽  
Vol 17 (1) ◽  
Author(s):  
Yang Lu ◽  
Jingchao Wang ◽  
Chen Dapeng ◽  
Di Wu ◽  
Guangyan Cai ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Proximal Tubule ◽  
Bioinformatics Analysis

CFTR channel insertion to the apical surface in rat duodenal villus epithelial cells is upregulated by VIP in vivo

1999 ◽  
Vol 112 (6) ◽  
pp. 887-894
Author(s):  
N.A. Ameen ◽  
B. Martensson ◽  
L. Bourguinon ◽  
C. Marino ◽  
J. Isenberg ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Apical Membrane ◽  
Surface Expression ◽  
Apical Plasma Membrane ◽  
Intracellular Camp ◽  
Apical Surface ◽  
C Terminus ◽  
Confocal Immunofluorescence ◽  
Small Intestinal Villus

cAMP activated insertion of the cystic fibrosis transmembrane conductance regulator (CFTR) channels from endosomes to the apical plasma membrane has been hypothesized to regulate surface expression and CFTR function although the physiologic relevance of this remains unclear. We previously identified a subpopulation of small intestinal villus epithelial cells or CFTR high expressor (CHE) cells possessing very high levels of apical membrane CFTR in association with a prominent subapical vesicular pool of CFTR. We have examined the subcellular redistribution of CFTR in duodenal CHE cells in vivo in response to the cAMP activated secretagogue vasoactive intestinal peptide (VIP). Using anti-CFTR antibodies against the C terminus of rodent CFTR and indirect immunofluorescence, we show by quantitative confocal microscopy that CFTR rapidly redistributes from the cytoplasm to the apical surface upon cAMP stimulation by VIP and returns to the cytoplasm upon removal of VIP stimulation of intracellular cAMP levels. Using ultrastructural and confocal immunofluorescence examination in the presence or absence of cycloheximide, we also show that redistribution was not dependent on new protein synthesis, changes in endocytosis, or rearrangement of the apical cytoskeleton. These observations suggest that physiologic cAMP activated apical membrane insertion and recycling of CFTR channels in normal CFTR expressing epithelia contributes to the in vivo regulation of CFTR mediated anion transport.

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