ArticleAmerican journal of physiology. Cell physiology2020
How goblet cells respond to dry eye: adaptive and pathological roles of voltage-gated calcium channels and P2X
Article in American journal of physiology. Cell physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Clinical observation of esculin and digitalisglycosides eye drops with 0.3% sodium hyaluronate eye drops for dry eye disease: a randomized controlled trial.Scientific reports · 2025Trial
- Lute-GenAntioxidants (Basel, Switzerland) · 2026Article
- Marine-Derived Neoagarotetraose Alleviates Dry Eye Disease by Suppressing Inflammation and Apoptosis in a Murine Model.Marine drugs · 2026Article
- Evaluation of ocular surface inflammation and systemic conditions in patients with systemic lupus erythematosus: a cross-sectional study.BMC ophthalmology · 2024Article
- Purinergic agonists increase [CaAmerican journal of physiology. Cell physiology · 2024Article
- Linarine inhibits inflammatory responses in dry eye disease mice by modulating purinergic receptors.Frontiers in immunology · 2024Article
- Impact of P2XInternational journal of molecular sciences · 2021Article
- Bioelectric Responses of Conjunctival Goblet Cells to Dry Eye: Impact of Ion Channels on Exocytotic Function and Viability.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Dry eye is a common sight-impairing, painful disorder characterized by disruption of the preocular tear film, whose integrity is required for ~70% of the eye's refractive power. A universal feature of clinical dry eye is hyperosmolarity of the tears resulting from their accelerated evaporation due to dysfunction of tear- and oil-producing ocular glands. A key adaptive response to dryness/hyperosmolarity is release of tear-stabilizing mucin by conjunctival goblet cells. Yet the mechanisms mediating this response to hyperosmolarity remain poorly understood. In this study of freshly excised rat conjunctiva, perforated-patch recordings revealed that during sustained hyperosmolarity, the development of a nonspecific cation (NSC) conductance depolarizes the goblet cells to a near-optimal voltage for the tonic activation of their voltage-gated calcium channels (VGCCs). In turn, as demonstrated by high-resolution membrane capacitance measurements, VGCC activation boosts the exocytotic response of conjunctival goblet cells to neural input. However, over time, VGCC activation also increases the vulnerability of these cells to the lethality of hyperosmolarity. Viability assays further revealed that hyperosmotic-induced goblet cell death is critically dependent on P2X
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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.