Evidence map›Paper›PMID 24940027›Full record

ArticleMolecular vision2014

Downregulation of Connexin 43 promotes vascular cell loss and excess permeability associated with the development of vascular lesions in the diabetic retina.

Thomas Tien, Tetsuya Muto, Kevin Barrette, Lucky Challyandra, Sayon Roy

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

38 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Skin capillary endothelial cells form a network of spatiotemporally conserved CaProceedings of the National Academy of Sciences of the United States of America · 2026
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  18. An Update on Connexin Gap Junction and Hemichannels in Diabetic Retinopathy.International journal of molecular sciences · 2021
    Review
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  20. Article
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

5 authors at 1 institution in 1 country.

Thomas TienDepartments of Medicine and Ophthalmology, Boston University School of Medicine, Boston, MA.
Tetsuya MutoDepartments of Medicine and Ophthalmology, Boston University School of Medicine, Boston, MA.
Kevin BarretteDepartments of Medicine and Ophthalmology, Boston University School of Medicine, Boston, MA.
Lucky ChallyandraDepartments of Medicine and Ophthalmology, Boston University School of Medicine, Boston, MA.
Sayon RoyDepartments of Medicine and Ophthalmology, Boston University School of Medicine, Boston, MA.
Boston University · US

Funding

Role of intercellular communication in pathogenesis of diabetic retinopathyR01EY018218 · NEI · BOSTON MEDICAL CENTER · PI ROY, SAYON · 2009 to 2021
$2.7M
NEI NIH HHS R01 EY018218NEI NIH HHS R01EY018218
6 · The paper itself

Abstract

purposeTo determine whether downregulation of Connexin 43 (Cx43) expression promotes development of acellular capillaries (ACs), pericyte loss (PL), excess permeability, and retinal thickening in rat retinas.

methodsControl rats, diabetic rats, and rats intravitreally injected with Cx43 siRNA or scrambled siRNA were used in this study to determine if acute downregulation of Cx43 expression contributes to retinal vascular cell death and excess permeability. Western blot (WB) analysis and Cx43 immunostaining were performed to assess Cx43 protein levels and distribution in the retinal vessels. Concurrently, retinal networks were subjected to terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling (TUNEL) assay and counter-stained to assess the number of apoptotic cells, ACs, and PL. Assessment of fluorescein isothiocyanate-dextran (FITC-dex) extravasation from retinal capillaries and optical coherence tomography (OCT) were performed to determine retinal vascular permeability and retinal thickness, respectively.

resultsWB analysis indicated a significant decrease in the Cx43 protein level in the retinas of the diabetic rats and those intravitreally injected with Cx43 siRNA compared to the retinas of the control rats. Likewise, the retinal vascular cells of the diabetic rats and the Cx43 siRNA-treated rats showed a significant decrease in Cx43 immunostaining. Importantly, the number of apoptotic cells, ACs and PL, FITC-dex extravasation, and thickness increased in the retinas of the diabetic and Cx43 siRNA-treated rats compared to those of the control rats.

conclusionsResults indicate that downregulation of Cx43 expression alone induces vascular cell death and promotes vascular permeability in the retina. These findings suggest that diabetes-induced downregulation of Cx43 participates in promoting retinal vascular lesions associated with diabetic retinopathy (DR).

Indexed as

Capillary PermeabilityDown-RegulationAnimalsApoptosisCapillariesConnexin 43Diabetic RetinopathyIntravitreal InjectionsMaleRatsRats, Sprague-DawleyRetinal VesselsRNA, Small InterferingConnexin 43RNA, Small Interfering

Identifiers

PMID24940027
PMCPMC4043608
OpenAlexW2153799033

What OpenQuestion 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 OpenQuestion graph.