epidermal-growth-factor and Cystic-Fibrosis

epidermal-growth-factor has been researched along with Cystic-Fibrosis* in 7 studies

Other Studies

7 other study(ies) available for epidermal-growth-factor and Cystic-Fibrosis

ArticleYear
Correlations of salivary biomarkers with clinical assessments in patients with cystic fibrosis.
    PloS one, 2015, Volume: 10, Issue:8

    Monitoring clinical disease status in cystic fibrosis frequently requires invasive collection of clinical samples. Due to its noninvasive collection process and direct anatomic relationship with the lower airway, saliva shows great potential as a biological fluid for cystic fibrosis monitoring.. To measure the levels of multiple protein markers in human saliva supernatants and investigate the possibility of utilizing them to provide a more quantitative measure of disease state for use in research and monitoring of patients with cystic fibrosis clinically.. Whole saliva samples were collected and processed from cystic fibrosis patients at two distinct time points (2010 and 2013) and measured by two separate platforms. In this cross sectional study, a convenience sample of 71 participants were recruited with samples measured by multiplexed fluorescence microarray (fiber microarray) and another 117 participant samples were measured by an automated, point-of-care, analyzer (SDReader) using a microsphere-based array via fluorescence sandwich immunoassay. For comparison, saliva from 56 and 50 healthy subjects were collected, respectively. The levels of six target proteins were quantified. Various demographic and clinical data, including spirometry, medical history, and clinicians' assessments were also collected from patients with cystic fibrosis on the day of saliva collection.. Similar trends were observed with both platforms and compared with healthy subjects, cystic fibrosis patients had significantly elevated levels of VEGF, IP-10, IL-8, and EGF as well as lower levels of MMP-9 (P ≤ 0.005) using fiber microarray and significantly elevated levels of IP-10, IL-8 with lower levels of MMP-9 and IL-1β (P ≤ 0.02) using the SDReader. The levels of the six proteins correlated with each other significantly, and in some cases, biomarker levels could be used to differentiate between subgroups of patients with different clinical presentations. For example, IP-10 levels significantly correlated with FEV1 and disease severity (as evaluated by clinicians) with both platforms (P < 0.05).. Significant variations of the levels of six proteins in saliva supernatants, and the correlations of these levels with clinical assessments, demonstrated the potential of saliva for cystic fibrosis research and monitoring.

    Topics: Adolescent; Adult; Aged; Biomarkers; Chemokine CXCL10; Child; Cross-Sectional Studies; Cystic Fibrosis; Epidermal Growth Factor; Female; Humans; Immunoassay; Interleukin-8; Longitudinal Studies; Male; Matrix Metalloproteinase 9; Middle Aged; Protein Array Analysis; Respiratory Function Tests; Saliva; Spirometry; Vascular Endothelial Growth Factor A

2015
Regulation of normal and cystic fibrosis airway epithelial repair processes by TNF-α after injury.
    American journal of physiology. Lung cellular and molecular physiology, 2011, Volume: 301, Issue:6

    Chronic infection and inflammation have been associated with progressive airway epithelial damage in patients with cystic fibrosis (CF). However, the effect of inflammatory products on the repair capacity of respiratory epithelia is unclear. Our objective was to study the regulation of repair mechanisms by tumor necrosis factor-α (TNF-α), a major component of inflammation in CF, in a model of mechanical wounding, in two bronchial cell lines, non-CF NuLi and CF CuFi. We observed that TNF-α enhanced the NuLi and CuFi repair rates. Chronic exposure (24-48 h) to TNF-α augmented this stimulation as well as the migration rate during repair. The cellular mechanisms involved in this stimulation were then evaluated. First, we discerned that TNF-α induced metalloproteinase-9 release, epidermal growth factor (EGF) shedding, and subsequent EGF receptor transactivation. Second, TNF-α-induced stimulation of the NuLi and CuFi wound-closure rates was prevented by GM6001 (metalloproteinase inhibitor), EGF antibody (to titrate secreted EGF), and EGF receptor tyrosine kinase inhibitors. Furthermore, we recently reported a relationship between the EGF response and K(+) channel function, both controlling bronchial repair. We now show that TNF-α enhances KvLQT1 and K(ATP) currents, while their inhibition abolishes TNF-α-induced repair stimulation. These results indicate that the effect of TNF-α is mediated, at least in part, through EGF receptor transactivation and K(+) channel stimulation. In contrast, cell proliferation during repair was slowed by TNF-α, suggesting that TNF-α could exert contrasting actions on repair mechanisms of CF airway epithelia. Finally, the stimulatory effect of TNF-α on airway wound repair was confirmed on primary airway epithelial cells, from non-CF and CF patients.

    Topics: Bronchioles; Cell Movement; Cell Proliferation; Cells, Cultured; Cystic Fibrosis; Epidermal Growth Factor; Epithelial Cells; ErbB Receptors; Humans; Matrix Metalloproteinase 9; Membrane Potentials; Phosphorylation; Potassium Channel Blockers; Potassium Channels; Primary Cell Culture; Quaternary Ammonium Compounds; Transcriptional Activation; Tumor Necrosis Factor-alpha

2011
EGF and K+ channel activity control normal and cystic fibrosis bronchial epithelia repair.
    American journal of physiology. Lung cellular and molecular physiology, 2008, Volume: 295, Issue:5

    Severe lesions of airway epithelia are observed in cystic fibrosis (CF) patients. The regulatory mechanisms of cell migration and proliferation processes, involved in the repair of injured epithelia, then need to be better understood. A model of mechanical wounding of non-CF (NuLi) and CF (CuFi) bronchial monolayers was employed to study the repair mechanisms. We first observed that wound repair, under paracrine and autocrine EGF control, was slower (up to 33%) in CuFi than in NuLi. Furthermore, EGF receptor (EGFR) activation, following wounding, was lower in CuFi than in NuLi monolayers. Cell proliferation and migration assays indicated a similar rate of proliferation in both cell lines but with reduced (by 25%) CuFi cell migration. In addition, cell migration experiments performed in the presence of conditioned medium, collected from NuLi and CuFi wounded bronchial monolayers, suggested a defect in EGF/EGFR signaling in CF cells. We (49) recently demonstrated coupling between the EGF response and K(+) channel function, which is crucial for EGF-stimulated alveolar repair. In CuFi cells, lower EGF/EGFR signaling was accompanied by a 40-70% reduction in K(+) currents and KvLQT1, ATP-sensitive potassium (K(ATP)), and Ca(2+)-activated K(+) (KCa3.1) channel expression. In addition, EGF-stimulated bronchial wound healing, cell migration, and proliferation were severely decreased by K(+) channel inhibitors. Finally, acute CFTR inhibition failed to reduce wound healing, EGF secretion, and K(+) channel expression in NuLi. In summary, the delay in CuFi wound healing could be due to diminished EGFR signaling coupled with lower K(+) channel function, which play a crucial role in bronchial repair.

    Topics: Bronchi; Cell Line; Cell Movement; Cell Proliferation; Cystic Fibrosis; Cystic Fibrosis Transmembrane Conductance Regulator; Epidermal Growth Factor; Epithelium; ErbB Receptors; Humans; Ion Channel Gating; Potassium Channels; Wound Healing

2008
Chronic exposure to EGF affects trafficking and function of ENaC channel in cystic fibrosis cells.
    Biochemical and biophysical research communications, 2005, Jun-03, Volume: 331, Issue:2

    Using the whole-cell patch-clamp technique, we identified an amiloride (AMI)-sensitive Na(+) current in cystic fibrosis cells, JME/CF15, growing in standard medium. The reversal potential of this current depended on Na(+) concentrations and the cation selectivity was much higher for Na(+) than for K(+), indicating that the current is through ENaC channels. In contrast, cells from EGF-containing medium lacked AMI-sensitive Na(+) currents. In permeabilized cells growing in EGF-containing medium, alphaENaC was mainly detected in a perinuclear region, while in cells from standard medium it was distributed over the cell body. Western-blot analysis showed that in standard medium cells expressed fast-migrating EndoH-insensitive and slow-migrating EndoH-sensitive alphaENaC fractions, while in cells growing in the presence of EGF, alphaENaC was only detected as the fast-migrating EndoH-insensitive fraction. Long-term incubation of cells with EGF resulted in an increased basal Ca(2+) level, [Ca(2+)](i). A similar increase of [Ca(2+)](i) was also observed in the presence of 2muM thapsigargin, resulting in inhibition of ENaC function. Thus, in JME/CF15 cells inhibition of the ENaC function by chronic incubation with EGF is a Ca(2+)-mediated process that affects trafficking and surface expression of ENaC channels.

    Topics: Calcium; Cells, Cultured; Cystic Fibrosis; Electric Conductivity; Epidermal Growth Factor; Epithelial Sodium Channels; Glycosylation; Humans; Ion Channel Gating; Ion Transport; Patch-Clamp Techniques; Protein Transport; Sodium; Sodium Channels; Thapsigargin; Time Factors

2005
Alterations of pancreatic amylase secretion in the reserpinized rat model of cystic fibrosis. Effects of cerulein and EGF.
    International journal of pancreatology : official journal of the International Association of Pancreatology, 1994, Volume: 16, Issue:1

    Reserpine treatment resulted in altered enzyme secretion from rat pancreatic acini in response to carbamylcholine and secretin (1,2). This study was undertaken: (1) To evaluate if the alterations caused by reserpine can be prevented by EGF and/or cerulein treatments; (2) To determine the time-course of secretion recovery after reserpine treatment; and (3) To establish if EGF and/or cerulein treatments can accelerate such a recovery after the reserpine treatment. Male Sprague-Dawley rats (250-265 g) were used in these experiments. In experiment I, rats divided into three groups received either reserpine (R) or the reserpine vehicle for the controls (C) and the pair-fed controls (PF) for 7 d. During treatment, PF and R rats were given SC, twice a day, saline, EGF (10 micrograms/kg), cerulein (1 microgram/kg), or both at the same dose. C rats received saline in gelatin. In experiment II, rats were treated for 7 d with reserpine or the vehicle as described in experiment I, were allowed a 30-d recovery period and then were killed. In experiment III, C, PF, and R rats were treated for 7 d as described in experiment I; on the 8th d and for the next 6 d, reserpine rats received saline (reserpine-saline), cerulein, EGF, or both cerulein +EGF at the same dose as indicated in experiment I. C and PF rats received saline in gelatin. After sacrifice, acini were prepared, and amylase dose-response curves to carbamylcholine (Cch) and secretin were established. EGF, cerulein, or their combination given to R rats did not improve the desensitized secretory response to Cch.(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: Amylases; Animals; Carbachol; Ceruletide; Cystic Fibrosis; Disease Models, Animal; Epidermal Growth Factor; Male; Pancreas; Rats; Rats, Sprague-Dawley; Reserpine; Secretin

1994
Cultured epithelial cells from patients with cystic fibrosis have an increased expression of the 14 kDa Ca2(+)-binding protein CFA.
    Biochemical and biophysical research communications, 1991, Feb-14, Volume: 174, Issue:3

    The Cystic Fibrosis antigen (CFA) is a 14 kDa. Ca2(+)-binding protein known to be expressed in cells of myeloid origin during normal cell differentiation. CFA serum levels are elevated in Cystic Fibrosis (CF) patients and heterozygotes. We examined the expression of CFA in different cultured epithelial cells from controls and patients with CF. The steady state level of CFA was in general higher in epithelial cells from CF patients compared to control cells and was found to increase during cell aging. The latter difference could be attributed to an increased rate of CFA synthesis rather than to an impairment of CFA degradation or secretion, as shown by pulse chase experiments.

    Topics: Blood Proteins; Calgranulin A; Cells, Cultured; Cystic Fibrosis; Cytoskeletal Proteins; Epidermal Growth Factor; Epithelium; Granulocytes; Humans; Immunoblotting; Kinetics; Molecular Weight; Nasal Polyps; Reference Values

1991
Saliva from cystic fibrosis patients contains an unusual form of epidermal growth factor.
    Biochemical and biophysical research communications, 1990, Aug-16, Volume: 170, Issue:3

    Epidermal Growth Factor (EGF) was assayed in saliva collected from control subjects and cystic fibrosis (CF) patients, using both radioimmuno (RIA) and radioreceptor (RRA) assays. An intriguing finding was that the average ratio of the values found by RRA over those obtained by RIA was of 1.7 for normal subjects and of about 0.4 for CF patients. This observation could be understood following gel filtration analysis of EGF-like material in these salivary fluids. Whereas control saliva contained the expected 6 kDa EGF active peptide, the immunoreactive EGF material from CF patients eluted as a polydisperse macromolecular moiety. The poor biological reactivity of this material as assessed by radioreceptor assay suggests that this EGF anomaly may contribute to the physiopathology of cystic fibrosis, especially as the upper gastrointestinal tract differentiated functions may be the target of normal salivary EGF.

    Topics: Adolescent; Child; Chromatography, Gel; Cystic Fibrosis; Epidermal Growth Factor; Humans; Radioimmunoassay; Radioligand Assay; Saliva

1990
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