scholarly journals FP016PARICALCITOL INHIBITED ALDOSTERONE-INDUCED PROINFLAMMATORY FACTORS BY MODULATING EPIDERMAL GROWTH FACTOR RECEPTOR PATHWAY IN CULTURED TUBULAR EPITHELIAL CELLS

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii71-iii71
Author(s):  
Jose Morgado-Pascual ◽  
Sandra Rayego-Mateos ◽  
Jose Valdivielso ◽  
Alberto Ortiz ◽  
Jesus Egido ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Growth Factor Receptor ◽  
Tubular Epithelial Cells ◽  
Epidermal Growth ◽  
Proinflammatory Factors

scholarly journals Paricalcitol Inhibits Aldosterone-Induced Proinflammatory Factors by Modulating Epidermal Growth Factor Receptor Pathway in Cultured Tubular Epithelial Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Jose L. Morgado-Pascual ◽  
Sandra Rayego-Mateos ◽  
Jose M. Valdivielso ◽  
Alberto Ortiz ◽  
Jesus Egido ◽  
...  
Keyword(s):  
Vitamin D ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Growth Factor Receptor ◽  
Tubular Epithelial Cells ◽  
Egfr Transactivation ◽  
Epidermal Growth ◽  
Anti Inflammatory ◽  
Proinflammatory Factors

Chronic kidney disease is characterized by Vitamin D deficiency and activation of the renin-angiotensin-aldosterone system. Increasing data show that vitamin D receptor agonists (VDRAs) exert beneficial effects in renal disease and possess anti-inflammatory properties, but the underlying mechanism remains unknown. Emerging evidence suggests that “a disintegrin and metalloproteinase” (ADAM)/epidermal growth factor receptor (EGFR) signalling axis contributes to renal damage. Aldosterone induces EGFR transactivation regulating several processes including cell proliferation and fibrosis. However, data on tubular epithelial cells is scarce. We have found that, in cultured tubular epithelial cells, aldosterone induced EGFR transactivation via TGF-α/ADAM17. Blockade of the TGF-α/ADAM17/EGFR pathway inhibited aldosterone-induced proinflammatory gene upregulation. Moreover, among the potential downstream mechanisms, we found that TGF-α/ADAM17/EGFR inhibition blocked ERK and STAT-1 activation in response to aldosterone. Next, we investigated the involvement of TGF-α/ADAM17/EGFR axis in VDRA anti-inflammatory effects. Preincubation with the VDRA paricalcitol inhibited aldosterone-induced EGFR transactivation, TGF-α/ADAM-17 gene upregulation, and downstream mechanisms, including proinflammatory factors overexpression. In conclusion, our data suggest that the anti-inflammatory actions of paricalcitol in tubular cells could depend on the inhibition of TGF-α/ADAM17/EGFR pathway in response to aldosterone, showing an important mechanism of VDRAs action.

scholarly journals Involvement of Epidermal Growth Factor Receptor-Linked Signaling Responses in Pseudomonas fluorescens-Infected Alveolar Epithelial Cells

2011 ◽  
Vol 79 (5) ◽  
pp. 1998-2005 ◽  
Author(s):  
Hye Jin Choi ◽  
Chan Hee Seo ◽  
Seong Hwan Park ◽  
Hyun Yang ◽  
Kee Hun Do ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Pseudomonas Fluorescens ◽  
Growth Factor Receptor ◽  
Airway Epithelial ◽  
Content Type ◽  
Proinflammatory Responses ◽  
Epidermal Growth

ABSTRACTPseudomonas fluorescensis an opportunistic indoor pathogen that can cause severe airway proinflammatory responses. Pulmonary epithelium, like other mucosal epithelial linings of the body, constitutes the first line of defense against airway microbial pathogens. Mucosal epithelial cells can be a sentinel of pathogenic bacteria via stimulation of specific cell surface receptors, including the epidermal growth factor receptor (EGFR) and Toll-like receptor (TLR). This study addressed the involvement of EGFR in airway epithelial pathogenesis byP. fluorescens. Human A549 pneumocytes showed prolonged production of proinflammatory interleukin-8 (IL-8) in response to infection withP. fluorescens, which was via the nuclear factor-kappa B (NF-κB) signaling pathway. Production of proinflammatory cytokine IL-8 was not mediated byP. fluorescenslipopolysaccharide, a representative TLR4 agonist, but was mediated through EGFR-linked signals activated by the opportunistic bacteria. Moreover, EGFR signals were involved in NF-κB signal-mediated production of proinflammatory cytokines. Along with persistent NF-κB activation,P. fluorescensenhanced the EGFR phosphorylation and subsequent activation of downstream mediators, including protein kinase B or extracellular-signal-regulated kinases 1/2. Blocking of EGFR-linked signals increased epithelial susceptibility to pathogen-induced epithelial cell death, suggesting protective roles of EGFR signals. Thus, airway epithelial exposure toP. fluorescenscan trigger antiapoptotic responses via EGFR and proinflammatory responses via TLR4-independent NF-κB signaling pathway in human pneumocytes.

scholarly journals Helicobacter pyloriInduces Up‐Regulation of the Epidermal Growth Factor Receptor in AGS Gastric Epithelial Cells

2007 ◽  
Vol 196 (1) ◽  
pp. 95-103 ◽  
Author(s):  
Sarah Keates ◽  
Andrew C. Keates ◽  
Kianoosh Katchar ◽  
Richard M. Peek, Jr. ◽  
Ciarán P. Kelly
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Growth Factor Receptor ◽  
Gastric Epithelial Cells ◽  
Epidermal Growth
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