Evidence map›Paper›PMID 21969293›Full record

ArticleInvestigative ophthalmology & visual science2011

Expression and functional roles of caspase-5 in inflammatory responses of human retinal pigment epithelial cells.

Zong-Mei Bian, Susan G Elner, Hemant Khanna, Carlos A Murga-Zamalloa, Suresh Patil, Victor M Elner

Open access · bronzeAbstract read
In one paragraph

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-weighted citation impact, top 21% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 46 citations in OpenAlex.

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  9. Crosstalk of the Caspase Family and Mammalian Target of Rapamycin Signaling.International journal of molecular sciences · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Zong-Mei BianDepartment of Ophthalmology, University of Michigan, Ann Arbor, Michigan 48105, USA.
Susan G Elner
Hemant Khanna
Carlos A Murga-Zamalloa
Suresh Patil
Victor M Elner
University of Michigan · US

Funding

VIVARIUM MODULEP30EY007003 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI David Antonetti · 1987 to 2026
$17.6M
RPE-Mphi Binding: Ca++_&O2-_Dependent AMD ResponsesR01EY009441 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELNER, VICTOR M · 1992 to 2008
$3.2M
E75 IN THE DEVELOPING DROSOPHILA EYEF31EY007003 · NEI · YALE UNIVERSITY · PI SHILTON, ALYCIA N · 1999 to 2001
$14k
NEI NIH HHS EY007003NEI NIH HHS EY-09441NEI NIH HHS F31 EY007003NEI NIH HHS P30 EY007003NEI NIH HHS R01 EY009441PHS HHS N007361
6 · The paper itself

Abstract

purposeTo investigate the expression, activation, and functional involvement of caspase-5 in human retinal pigment epithelial (hRPE) cells.

methodsExpression and activation of caspase-5 in primary cultured hRPE cells, telomerase-immortalized hTERT-RPE1 cells (hTERT-RPE1), or both, were measured after stimulation with proinflammatory agents IL-1β, TNF-α, lipopolysaccharide (LPS), interferon-γ, monocyte coculture, adenosine triphosphate (ATP), or endoplasmic reticulum (ER) stress inducers. Immunomodulating agents dexamethasone (Dex), IL-10, and triamcinolone acetonide (TA) were used to antagonize proinflammatory stimulation. Cell death ELISA and TUNEL staining assays were used to assess apoptosis.

resultsCaspase-5 mRNA expression and protein activation were induced by LPS and monocyte-hRPE coculture. Caspase-5 activation appeared as early as 2 hours after challenge by LPS and consistently increased to 24 hours. Meanwhile, caspase-1 expression and protein activation were induced by LPS. Activation of caspase-5 was blocked or reduced by Dex, IL-10, and TA. Activation of caspase-5 and -1 was also enhanced by ATP and ER stress inducers. Expression and activation of caspase-5 were inhibited by a caspase-1-specific inhibitor. Caspase-5 knockdown reduced caspase-1 protein expression and activation and inhibited TNF-α-induced IL-8 and MCP-1. In contrast to caspase-4, the contribution of caspase-5 to stress-induced apoptosis was moderate.

conclusionsCaspase-5 mRNA synthesis, protein expression, and catalytic activation were highly regulated in response to various proinflammatory stimuli, ATP, and ER stress inducers. Mutual activation between caspase-5 and -1 suggests caspase-5 may work predominantly in concert with caspase-1 in modulating hRPE inflammatory responses.

Indexed as

Adenosine TriphosphateAnti-Inflammatory AgentsApoptosisCaspase 1CaspasesCells, CulturedChemokine CCL2Coculture TechniquesDexamethasoneEndoplasmic Reticulum StressEpithelial CellsGene ExpressionGene Knockdown TechniquesHumansInterferon-gammaInterleukin-10Adenosine TriphosphateAnti-Inflammatory AgentsCASP5 protein, humanCaspase 1CaspasesCCL2 protein, humanChemokine CCL2DexamethasoneIL10 protein, humanInterferon-gammaInterleukin-10LipopolysaccharidesTriamcinoloneTumor Necrosis Factor-alpha

Identifiers

PMID21969293
PMCPMC3230287
OpenAlexW1974708450

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.