Document Detail


TRPV1 activation is required for hypertonicity-stimulated inflammatory cytokine release in human corneal epithelial cells.
MedLine Citation:
PMID:  20739465     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: To determine whether hypertonic stress promotes increases in inflammatory cytokine release through transient receptor potential vanilloid channel type 1 (TRPV1) signaling pathway activation in human corneal epithelial cells (HCECs).
METHODS: Hyperosmotic medium was prepared by supplementing isotonic Ringers solution with sucrose. Ca2+ signaling was measured in fura2-AM-loaded HCECs using a single-cell fluorescence imaging system. Western blot analysis evaluated the phosphorylation status of EGFR, ERK, p38 MAPK, and nuclear factor (NF)-κB. ELISA assessed the effect of TRPV1 activation on the release of IL-6 and IL-8.
RESULTS: A 450 mOsm hypertonic stress elicited 2-fold Ca2+ transients that were suppressed by the TRPV1-selective antagonists capsazepine and JYL 1421. Such transients were enhanced by PGE2. Hypertonicity-induced EGF receptor (EGFR) transactivation was suppressed by preincubating HCECs with capsazepine, matrix metalloproteinase 1 (MMP1) inhibitor TIMP-1, broad-spectrum MMP inhibitor GM 6001, heparin-bound (HB)-EGF inhibitor CRM 197, or EGFR inhibitor AG 1478. ERK and p38 MAPK and NF-κB activation after EGFR transactivation occurred in tonicity and in a time-dependent manner. Hypertonicity-induced increases in IL-6 and IL-8 releases were suppressed by exposure to capsazepine, AG 1478, ERK inhibitor PD 98059, p38 inhibitor SB 203580, or NF-κB inhibitor PDTC.
CONCLUSIONS: Hypertonic stress-elicited TRPV1 channel stimulation mediates increases in a proinflammatory cytokine IL-6 and a chemoattractant IL-8 by eliciting EGFR transactivation, MAPK, and NF-κB activation. Selective drug modulation of either TRPV1 activity or its signaling mediators may yield a novel approach to suppressing inflammatory responses occurring in dry eye syndrome.
Authors:
Zan Pan; Zheng Wang; Hua Yang; Fan Zhang; Peter S Reinach
Related Documents :
16705145 - Nitric oxide stimulates cox-2 expression in cultured collecting duct cells through map ...
1705005 - Interleukin-6 signals activating junb and tis11 gene transcription in a b-cell hybridoma.
20201075 - Meta060 inhibits osteoclastogenesis and matrix metalloproteinases in vitro and reduces ...
10720495 - Autocrine/paracrine secretion of il-6 family cytokines causes angiotensin ii-induced de...
17017875 - Protein tyrosine phosphatases, new targets for cancer therapy.
18566245 - Photodynamic therapy with an endocytically located photosensitizer cause a rapid activa...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-01-21
Journal Detail:
Title:  Investigative ophthalmology & visual science     Volume:  52     ISSN:  1552-5783     ISO Abbreviation:  Invest. Ophthalmol. Vis. Sci.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-24     Completed Date:  2011-02-25     Revised Date:  2011-08-01    
Medline Journal Info:
Nlm Unique ID:  7703701     Medline TA:  Invest Ophthalmol Vis Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  485-93     Citation Subset:  IM    
Affiliation:
Department of Biological Sciences, College of Optometry, State University of New York, New York, New York 10065, USA. zap2001@med.cornell.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Blotting, Western
Calcium / metabolism
Capsaicin / analogs & derivatives,  pharmacology
Cells, Cultured
Enzyme Inhibitors / pharmacology
Enzyme-Linked Immunosorbent Assay
Epithelium, Corneal / drug effects*,  metabolism
Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors,  metabolism
Fura-2 / analogs & derivatives
Humans
Hypertonic Solutions / pharmacology*
Interleukin-6 / metabolism*
Interleukin-8 / metabolism*
Microscopy, Fluorescence
NF-kappa B / antagonists & inhibitors,  metabolism
Phosphorylation
Receptor, Epidermal Growth Factor / metabolism
Signal Transduction
Stress, Physiological
Sulfonamides / pharmacology
TRPV Cation Channels / antagonists & inhibitors,  metabolism*
Thiourea / analogs & derivatives,  pharmacology
Time Factors
p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors,  metabolism
Grant Support
ID/Acronym/Agency:
EY04795/EY/NEI NIH HHS
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Hypertonic Solutions; 0/Interleukin-6; 0/Interleukin-8; 0/JYL 1421; 0/NF-kappa B; 0/Sulfonamides; 0/TRPV Cation Channels; 0/TRPV1 protein, human; 0/capsazepine; 105344-37-4/fura-2-am; 404-86-4/Capsaicin; 62-56-6/Thiourea; 7440-70-2/Calcium; 96314-98-6/Fura-2; EC 2.7.10.1/EGFR protein, human; EC 2.7.10.1/Receptor, Epidermal Growth Factor; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Arp2/3- and cofilin-coordinated actin dynamics is required for insulin-mediated GLUT4 translocation ...
Next Document:  Spontaneous lymphatic vessel formation and regression in the murine cornea.