TRPV1 Activation Is Required for Hypertonicity-Stimulated Inflammatory Cytokine Release in Human Corneal Epithelial Cells

Pan, Zhongdang; Wang, Zheng; Yang, Hua; Zhang, Fan; Reinach, Peter S.

doi:10.1167/iovs.10-5801

Cited by 125 publications

(100 citation statements)

References 53 publications

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“…TRPV1-induces downstream events by eliciting time dependent stimulation of the mitogen activated protein kinase (MAPK) cascade in epithelial cells and stromal fibroblasts (79,81) . Corneal epithelial wound is also accompanied by increased release of mitogens such as, epidermal growth factor (EGF), which induces cell proliferation and migration through activation of a TRP channel in the canonical subfamily identified as TRPC4 and MAPK signaling pathway (82)(83)(84)(85) . Flow cytometry analysis of the tear fluid collected from the individuals with atopic keratoconjunctivitis after a conjunctival allergen provocation test presented higher levels of interferon-gamma, IL-6, and a borderline increase in IL-10 after 48 hours.…”

Section: Epidemiology Of Dry Eye Related To Environmental Factorsmentioning

confidence: 99%

Is dry eye an environmental disease?

Alves¹,

Novaes²,

Morraye³

et al. 2014

Arquivos Brasileiros De Oftalmologia

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Previous studies have revealed that eye contact with either air pollutants or adverse indoor and/or outdoor environmental conditions can affect tear film composition and ocular surface components. These effects are mediated by selective binding of the environmental agents to ocular surface membrane receptors, leading to activation of pro inflammatory signaling pathways. The aim of the current review was to examine the published evidence associated with environmental factors and ocular surface disease and dry eye. Specifically, the reader will appreciate why it is possible to refer to them as mediators of Environmental Dry Eye Disease (EDED), a singular clinical entity inside DED context, directly caused by pollutants and/ or adverse climatic conditions. The indicators and clinical findings are described along with EDE differential diagnosis in its acute and the chronic phases. Based on strong existing evidence of clinical reports and epidemiological observations regarding DED and environmental factors we conclude that there is a straight cause-and-effect relationship between ambient stresses and DED. International standards and web-based tools are described for monitoring worldwide environmental conditions referring localities and populations susceptible to EDED. This information is beneficial to health providers to pinpoint the individuals and predisposed groups afflicted with DED. Such insights may not only improve the understanding and treatment of DED but also help to identify the contributing factors and lower the frequency and progression of EDED. of DED has been studied and confirmed in animal models of human DED (13)(14)(15) . KeywordsAs indicated, a healthy and pain-free ocular surface depends on identifying and eliminating factors that cause ambient humidity, airflow and purity, and temperature to intolerable levels. Such an undertaking is needed to preserve tear film qualities commensurate with ocular surface health. This is essential to sustain sufficient corneal refractive power, visual acuity, and ocular comfort (5,16,17) . A desiccating environment can lead to increase in tear film evaporation and/or decline in its turn over and clearance. These initial events lead to exposure of the ocular surface to hazardous environmental elements that trigger or exacerbate EDED symptoms. Clinical findings have shown that increased numbers of people are affected by EDED because of exposure to environmental factors ( Figure 2).Our purpose herein is to provide a critical appraisal of the clinical and epidemiological evidence indicating that DED is influenced by environmental factors. Secondly, we delineate EDED as a single clinical entity with a unique set of symptoms and clinical findings different from that of either DED or other diseases, such as Sjögren's syndrome, diabetes mellitus or drug induced, allergic conjunctivitis, toxic or irritative conjunctivitis, and actinic keratitis. Moreover, we will describe standard tools used to monitor environmental conditions and discuss their relevance in EDED ep...

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Section: Epidemiology Of Dry Eye Related To Environmental Factorsmentioning

confidence: 99%

Is dry eye an environmental disease?

Alves¹,

Novaes²,

Morraye³

et al. 2014

Arquivos Brasileiros De Oftalmologia

View full text Add to dashboard Cite

show abstract

“…It has been shown that the application of NaCl, capsicum, and nicotine into the corneal surface produce a vigorous response in the nociceptive neurons in the trigeminal subnucleus caudalis in rat [20]. Hyperosmotic solution like NaCl by activating transient receptor potential (TRP) vanilloid 1 and TRP melastatin 8 receptors on corneal nociceptors could induce chemical nociception [21,22].…”

Section: Discussionmentioning

confidence: 99%

The Effect of Histamine H1 Receptor Antagonists on the Morphine-Induced Antinociception in the Acute Trigeminal Model of Nociception in Rats

Khalilzadeh

Azarpey

Hazrati

2016

Asian J Pharm Clin Res

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Objective: In this study, the effect of different classes of histamine H 1 receptor antagonists (chlorpheniramine, cetirizine, and fexofenadine), µ opioid receptor agonist (morphine), and opioid receptor antagonist (naloxone) in separate and combined treatments were investigated on the acute trigeminal model of pain in rats.Methods: Eye wiping test used for induction of acute trigeminal pain by putting a drop of NaCl, 5 M solution (40 µl) on the corneal surface of the eye, and the number of eye wipes counted during the first 30 seconds.Results: Intraperitoneal injection of both chlorpheniramine and cetirizine at doses of 10 and 20 mg/kg significantly inhibited the acute trigeminal pain. However, fexofenadine did not change corneal pain response. Morphine at doses of 1.25, 2.5, and 5 mg/kg reduced eye wipe responses. Administration of both chlorpheniramine and cetirizine but not fexofenadine before morphine-enhanced morphine analgesic activity, also pretreatment of animals with naloxone inhibited morphine, chlorpheniramine, and cetirizine-induced analgesia in the acute corneal pain. Conclusion:Our results showed that chlorpheniramine as a histamine H 1 antagonist that efficiently Penetrates blood-brain barrier (BBB) and cetirizine with less penetration of BBB but not fexofenadine (an H 1 receptor antagonist with a negligible brain-accessibility) could induce analgesia in the acute corneal pain via opioidergic mechanism. Coadministration of morphine with chlorpheniramine or cetirizine could enhance its analgesic activity in the acute trigeminal model of pain in rats.

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“…TRPV1, TRPV2, TRPV3 and TRPV4 channels are expressed in the cornea whereas TRPV1, TRPV2, TRPV5 and TRPV6 channels are expressed in the retina. [15][16][17][18][19][20] The TRPA channel subfamily has only one member, TRPA1. Fig.…”

Section: Wwwintechopencommentioning

confidence: 99%

“…Transient increases in intracellular calcium concentration trigger intracellular activation of mediators including: 1) phospholipase C (PLC) by coupled GTP-binding protein, leading to stimulation of storeoperated Ca 2+ channels; 2) transactivation of EGF tyrosine receptors through MMPmediated HB-EGF shedding. 4,10,16 The physiological significance of TRP channel expression is indicated by the finding that TRP channel mutations are linked to human diseases. 22 There is compelling evidence that the TRP channel superfamily plays a critical role in ocular homeostasis and pathogenesis.…”

Section: Wwwintechopencommentioning

confidence: 99%

“…On the other hand, pre-exposure to a selective TRPV1 channel antagonist obviated all of these responses, suggesting that TRPV1 channels are potential drug target for the treatment of dry eye syndrome because suppression of its activation may reduce ocular surface inflammation. 16,23 In contrast with TRPV1, its cohort, TRPV4 channel reacts to a different spectrum of stresses. Unlike TRPV1, which is thought to only be activated by a hyperosmolar stress, TRPV4 channels may instead be an osmosensor for a hypoosmolar challenge.…”

Section: Roles Of Trp Channels In Corneal Sensation and Wound Healingmentioning

confidence: 99%

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