Evidence map›Paper›PMID 32121610›Full record

ArticleInternational journal of molecular sciences2020

Extracellular Vesicle-Induced Classical Complement Activation Leads to Retinal Endothelial Cell Damage via MAC Deposition.

Chao Huang, Kiera P Fisher, Sandra S Hammer, Julia V Busik

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  3. Article
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  5. Article
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  8. Review
  9. Salivary Exosomes in Health and Disease: Future Prospects in the Eye.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Emerging Role of Exosomes in Retinal Diseases.Frontiers in cell and developmental biology · 2021
    Review
  17. Extracellular vesicles: new players in regulating vascular barrier function.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  18. Review
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

4 authors at 1 institution in 1 country.

Chao HuangDepartment of Physiology, Michigan State University, East Lansing, MI 48824, USA.
Kiera P FisherDepartment of Physiology, Michigan State University, East Lansing, MI 48824, USA.
Sandra S HammerDepartment of Physiology, Michigan State University, East Lansing, MI 48824, USA.
Julia V BusikDepartment of Physiology, Michigan State University, East Lansing, MI 48824, USA.ORCID 0000-0003-3453-7124
Michigan State University · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
LXR as a Novel Therapeutic Target in Diabetic RetinopathyR01EY025383 · NEI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BUSIK, JULIA V, GRANT, MARIA BARTOLOMEO · 2015 to 2024
$4.2M
Michigan Experimental Agricultural Station MICL02163NIDDK NIH HHS P30 DK020572NIH HHS R01EY025383NIH HHS RO1EY016077
6 · The paper itself

Abstract

Several studies have suggested that there is a link between membrane attack complex (MAC) deposition in the retina and the progression of diabetic retinopathy (DR). Our recent investigation demonstrated that circulating IgG-laden extracellular vesicles contribute to an increase in retinal vascular permeability in DR through activation of the complement system. However, the mechanism through which extracellular vesicle-induced complement activation contributes to retinal vascular cytolytic damage in DR is not well understood. In this study, we demonstrate that IgG-laden extracellular vesicles in rat plasma activate the classical complement pathway, and in vitro Streptozotocin (STZ)-induced rat diabetic plasma results in MAC deposition and cytolytic damage in human retinal endothelial cells (HRECs). Moreover, removal of the plasma extracellular vesicles reduced the MAC deposition and abrogated cytolytic damage seen in HRECs. Together, the results of this study demonstrate that complement activation by IgG-laden extracellular vesicles in plasma could lead to MAC deposition and contribute to endothelium damage and progression of DR.

Indexed as

AnimalsCell DeathCell SurvivalComplement ActivationComplement C1Complement Membrane Attack ComplexDiabetes Mellitus, ExperimentalEndothelial CellsExtracellular VesiclesHumansImmunoglobulinsMaleRats, Sprague-DawleyRetinaComplement C1Complement Membrane Attack ComplexImmunoglobulinscomplement systemdiabetic retinopathyextracellular vesicleshuman retinal endothelial cells (HRECs)membrane attack complex (MAC)retinal vascular damage

Identifiers

PMID32121610
PMCPMC7084203
OpenAlexW3009157579

What OpenQuestion holds

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LicenceCC BY
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.