ArticleInvestigative ophthalmology & visual science2011
sPLA2-IIa amplifies ocular surface inflammation in the experimental dry eye (DE) BALB/c mouse model.
Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Tear cytokine profile as a noninvasive biomarker of inflammation for ocular surface diseases: standard operating procedures.Investigative ophthalmology & visual science · 2013Trial
- Tear proteomic analysis in keratoconus patients and potential biomarkers: a case-control study.Experimental biology and medicine (Maywood, N.J.) · 2025Observational
- A Mouse Model for Ocular Surface Staphylococcus aureus Infection.Current protocols in mouse biology · 2017Article
- Longitudinal changes in tear fluid lipidome brought about by eyelid-warming treatment in a cohort of meibomian gland dysfunction.Journal of lipid research · 2014Article
- Secretory phospholipase A2 enzymes as pharmacological targets for treatment of disease.Biochemical pharmacology · 2014Review
- Set-based joint test of interaction between SNPs in the VEGF pathway and exogenous estrogen finds association with age-related macular degeneration.Investigative ophthalmology & visual science · 2014Article
- The core mechanism of dry eye disease is inflammation.Eye & contact lens · 2014Review
- Oleanolic acid controls allergic and inflammatory responses in experimental allergic conjunctivitis.PloS one · 2014Article
- Dry eye disease and microbial keratitis: is there a connection?The ocular surface · 2013Review
- Toll-like receptor expression and activation in mice with experimental dry eye.Investigative ophthalmology & visual science · 2013Article
- Surfactant protein D contributes to ocular defense against Pseudomonas aeruginosa in a murine model of dry eye disease.PloS one · 2013Article
- Neurotransmitter influence on human meibomian gland epithelial cells.Investigative ophthalmology & visual science · 2011Article
- Dry eye syndrome model established in rabbits via mitomycin C injection in the lacrimal gland.Taiwan journal of ophthalmologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
purposesPLA2-IIa is a biomarker for many inflammatory diseases in humans and is found at high levels in human tears. However, its role in ocular surface inflammation remains unclear. An experimentally induced BALB/c mouse dry eye (DE) model was used to elucidate the role of sPLA2-IIa in ocular surface inflammation.
methodsBALB/c mice were subcutaneously injected with scopolamine and placed in a daytime air-drying device for 5 to 10 days. Control mice received no treatment. DE status was evaluated with tear production with a phenol-red thread method. Tear inflammatory cytokines were quantified by multiplex immunoassays. Ocular surface inflammation and sPLA2-IIa expression were examined by immune-staining and quantitative (q)RT(2)-PCR. Conjunctiva (CNJ) of the mice was cultured for prostaglandin E2 production induced by sPLA2-IIa with various amount of sPLA2-IIa inhibitor, S-3319.
resultsTreated mice produced fewer tears and heavier corneal (CN) fluorescein staining than the untreated controls (P < 0.001). They also revealed lower goblet cell density (P < 0.001) with greater inflammatory cell infiltration within the conjunctiva, and higher concentration of tear inflammatory cytokines than the controls. Moreover, treated mice showed heavier sPLA2-IIa immune staining than the controls in the CNJ epithelium, but not in the CN epithelium or the lacrimal gland. Treated mice exhibited upregulated sPLA2-IIa and cytokine gene transcription. Furthermore, CNJ cultures treated with sPLA2-IIa inhibitor showed significantly reduced sPLA2-IIa-induced inflammation.
conclusionsThis is the first report regarding sPLA2-IIa in the regulation of ocular surface inflammation. The findings may therefore lead to new therapeutic strategies for ocular surface inflammation, such as DE disease.
Indexed as
Identifiers
What 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.