ArticleMolecular vision2009
Hypoxia-altered signaling pathways of toll-like receptor 4 (TLR4) in human corneal epithelial cells.
Article in Molecular vision, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Aspergillus fumigatus Hypoxia Adaptation Is Critical for the Establishment of Fungal Keratitis.Investigative ophthalmology & visual science · 2024Article
- Effects of hypoxia in the diabetic corneal stroma microenvironment.Experimental eye research · 2024Article
- Glycosaminoglycans: Roles in wound healing, formation of corneal constructs and synthetic corneas.The ocular surface · 2023Review
- Hypoxia adaptation in the cornea: Current animal models and underlying mechanisms.Animal models and experimental medicine · 2021Review
- Foundational concepts in the biology of bacterial keratitis.Experimental eye research · 2021Review
- The Role of Hypoxia in Corneal Extracellular Matrix Deposition and Cell Motility.Anatomical record (Hoboken, N.J. : 2007) · 2020Article
- Analysis of differentially expressed genes in bacterial and fungal keratitis.Indian journal of ophthalmology · 2020Article
- Controls of Nuclear Factor-Kappa B Signaling Activity by 5'-AMP-Activated Protein Kinase Activation With Examples in Human Bladder Cancer Cells.International neurourology journal · 2016Review
- Review
- Hypoxic Stress Induced TREM-1 and Inflammatory Chemokines in Human Peripheral Blood Mononuclear Cells.Indian journal of clinical biochemistry : IJCB · 2014Article
- Regulation of Toll-like receptor expression in human conjunctival epithelial cells.Mediators of inflammation · 2014Article
- Hypoxia preconditioning increases survival and decreases expression of Toll-like receptor 4 in pulmonary artery endothelial cells exposed to lipopolysaccharide.Pulmonary circulation · 2013Article
- Acanthamoeba-cytopathic protein induces apoptosis and proinflammatory cytokines in human corneal epithelial cells by cPLA2α activation.Investigative ophthalmology & visual science · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeToll-like receptor 4 (TLR4), a member of the TLR family, is an important pattern recognition molecule that plays a role in the host's innate immune responses to lipopolysaccharide (LPS), a component of gram-negative bacteria. Contact lens wear is one of the risk factors for bacterial keratitis. The purpose of this study was to determine whether hypoxia or contact lens wear alters the TLR4 signaling pathways in human corneal epithelial cells (HCECs).
methodA simian virus 40-immortalized human corneal epithelial cell (SV40-HCEC) line was cultured under 20% O2 or 2% O2 and exposed to LPS. The expression of TLR4, interleukin-6 (IL-6), and IL-8 was determined using a real-time reverse transcription-polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), and immunoblotting. Immunoblotting was also used to determine whether the nuclear factor kappa B (NFkappaB) was activated in the SV40-HCEs. HCECs were obtained from 17 healthy volunteers and 18 hydrogel soft contact lens (SCL) wearers using impression cytology (IC), and the expression of the mRNA of TLR4 was determined using real-time RT-PCR.
resultsA reduction in the expression of the mRNA and protein of TLR4 was detected in SV40-HCECs cultured under hypoxic conditions. Hypoxia also attenuated both the LPS-induced expression of IL-6 and IL-8, and the activation of NFkappaB in SV40-HCECs. The expression of the mRNA of TLR4 was down-regulated in the HCECs of soft contact lens wearers.
conclusionsThese results indicate that hypoxia attenuates the TLR4 signaling pathway in HCECs, suggesting that the increase in the susceptibility to bacterial infections under hypoxic conditions may be related to the TLR4 signaling pathways.
Indexed as
Identifiers
19960069PMC2787305W2141726839What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.