Evidence map›Paper›PMID 36531590›Full record

ArticleOphthalmology science2022

Cellular Interplay Through Extracellular Vesicle miR-184 Alleviates Corneal Endothelium Degeneration.

Tomoko Yamashita, Kazuko Asada, Morio Ueno, Nao Hiramoto, Tomoko Fujita, Munetoyo Toda, Chie Sotozono, Shigeru Kinoshita, Junji Hamuro

Open access · goldAbstract read
In one paragraph

Article in Ophthalmology science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. miR-184 in hepatocellular carcinoma: a promising therapeutic target.Journal of physiology and biochemistry · 2025
    Review
  3. Review
  4. Article
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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

9 authors at 1 institution in 1 country.

Tomoko YamashitaDepartment of Frontier Medical Science and Technology for Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Kazuko AsadaDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Morio UenoDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Nao HiramotoDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Tomoko FujitaDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Munetoyo TodaDepartment of Frontier Medical Science and Technology for Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Chie SotozonoDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Shigeru KinoshitaDepartment of Frontier Medical Science and Technology for Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Junji HamuroDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Kyoto Prefectural University of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: The objective of the study was to reveal the presence of cellular interplay through extracellular vesicle (EV) microRNAs (miRs), to dampen the vicious cycle to degenerate human corneal endothelium (HCE) tissues. Design: Prospective, comparative, observational study. Methods: The miR levels in neonate-derived corneal tissues, in the aqueous humor (AqH) of bullous keratoplasty and cataract patients, as well as in the culture supernatant (CS) and EV of cultured human corneal endothelial cells (hCECs), were determined using 3D-Gene human miR chips and then validated using the real-time polymerase chain reaction. The extracellularly released miRs were profiled after the forced downregulation of cellular miR-34a, either by an miR-34a inhibitor or exposure to H Main Outcome Measures: Identification of functional miRs attenuating HCE degeneration. Results: The miRs in AqH were classified into 2 groups: expression in 1 group was significantly reduced in neonate-derived tissues, whereas that in the other group remained almost constant, independent of aging. The miR-34a and -29 families were typical in the former group, whereas miR-184 and -24-3p were typical in the latter. Additionally, a larger amount of the latter miRs was detected in AqH compared with those of the former miRs. There was also a greater abundance of miR-184 and -24-3p in hCECs, EV, and CS in fully mature CD44 Conclusions: The elevated release of miR-184 into AqH may constitute cellular interplay that prevents the aggravation of HCE degeneration induced by oxidative stress, thereby sustaining tissue homeostasis in HCE.

Indexed as

AqH, aqueous humorAQP-1, aquaporin 1Corneal endothelium degenerationCS, culture supernatantECD, endothelial cell densityER, endoplasmic reticulumEV, extracellular vesicleExtracellular vesiclehCEC, cultured human corneal endothelial cellHCE, human corneal endotheliumIL-6, interleukin 6MCP-1, monocyte chemotactic protein-1MiR-184miR, microRNAMitochondria metabolic homeostasisMMP, mitochondrial membrane potentialOxidative stressSASP, senescence-associated secretory phenotypeSLC4A11, solute carrier family 4 member 11SP, subpopulation

Identifiers

PMID36531590
PMCPMC9755023
OpenAlexW4292411365

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.