Evidence map›Paper›PMID 22772798›Full record

ArticleDiabetologia2012

Reduction of experimental diabetic vascular leakage and pericyte apoptosis in mice by delivery of αA-crystallin with a recombinant adenovirus.

Y H Kim, S Y Park, J Park, Y S Kim, E M Hwang, J Y Park, G S Roh, H J Kim, S S Kang, G J Cho and 1 more

Open access · bronzeAbstract read
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In one paragraph

Article in Diabetologia, 2012. 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
2.9field-weighted citation impact, top 9% 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, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Small Heat Shock Proteins in Retinal Diseases.Frontiers in molecular biosciences · 2022
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Therapeutic potential of α-crystallin.Biochimica et biophysica acta · 2016
    Review
  15. Article
  16. Article
  17. 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

11 authors at 2 institutions in 1 country.

Y H KimDepartment of Anatomy and Neurobiology, Medical Research Center for Neural Dysfunction, Institute of Health Science, School of Medicine, Gyeongsang National University, 92 Chilam-dong, Jinju, Gyeongnam, 660-751, Republic of Korea.
S Y ParkDepartment of Anatomy and Neurobiology, Medical Research Center for Neural Dysfunction, Institute of Health Science, School of Medicine, Gyeongsang National University, 92 Chilam-dong, Jinju, Gyeongnam, 660-751, Republic of Korea.
J ParkDepartment of Anatomy and Neurobiology, Medical Research Center for Neural Dysfunction, Institute of Health Science, School of Medicine, Gyeongsang National University, 92 Chilam-dong, Jinju, Gyeongnam, 660-751, Republic of Korea.
Y S KimDepartment of Anatomy and Neurobiology, Medical Research Center for Neural Dysfunction, Institute of Health Science, School of Medicine, Gyeongsang National University, 92 Chilam-dong, Jinju, Gyeongnam, 660-751, Republic of Korea.
E M HwangCenter for Functional Connectomics, Korea Institute of Science and Technology, Seoul, Republic of Korea.
J Y ParkDepartment of Physiology, School of Medicine, Gyeongsang National University, Jinju, Republic of Korea.
G S RohDepartment of Anatomy and Neurobiology, Medical Research Center for Neural Dysfunction, Institute of Health Science, School of Medicine, Gyeongsang National University, 92 Chilam-dong, Jinju, Gyeongnam, 660-751, Republic of Korea.
H J KimDepartment of Anatomy and Neurobiology, Medical Research Center for Neural Dysfunction, Institute of Health Science, School of Medicine, Gyeongsang National University, 92 Chilam-dong, Jinju, Gyeongnam, 660-751, Republic of Korea.
S S KangDepartment of Anatomy and Neurobiology, Medical Research Center for Neural Dysfunction, Institute of Health Science, School of Medicine, Gyeongsang National University, 92 Chilam-dong, Jinju, Gyeongnam, 660-751, Republic of Korea.
G J ChoDepartment of Anatomy and Neurobiology, Medical Research Center for Neural Dysfunction, Institute of Health Science, School of Medicine, Gyeongsang National University, 92 Chilam-dong, Jinju, Gyeongnam, 660-751, Republic of Korea.
W S ChoiDepartment of Anatomy and Neurobiology, Medical Research Center for Neural Dysfunction, Institute of Health Science, School of Medicine, Gyeongsang National University, 92 Chilam-dong, Jinju, Gyeongnam, 660-751, Republic of Korea. choiws@gnu.ac.kr.
Gyeongsang National University · KRKorea Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisThe study aimed to evaluate the efficacy of recombinant adenovirus expressing αA-crystallin (Ad-αAc-Gfp) in reducing pericyte loss within retinal vasculature in early diabetes.

methodsDiabetes was induced by streptozotocin injection into C57BL/6 mice. Ad-αAc-Gfp was delivered by intravitreous injection to the right eyes of mice 2 weeks before induction of diabetes. Vascular leakage was determined by fluorescent angiography, Evans Blue leakage assay and leucocyte adhesion test. Production of αA-crystallin was analysed by immunoblotting and double immunostaining and pericyte loss was analysed by pericyte count.

resultsVessel leakage and pericyte loss were observed in the streptozotocin-induced diabetic retina. Decreased abundance of αA-crystallin in retinas 2 and 6 months after the induction of diabetes was confirmed by two-dimensional electrophoretic analysis, immunoblotting and RT-PCR. Double immunofluorescence staining for αA-crystallin and NG2 chondroitin sulphate proteoglycan revealed that αA-crystallin was predominantly produced in the retinal pericyte and that the number of αA-crystallin-producing pericytes decreased in the diabetic retina. Retinal infection with Ad-αAc-Gfp led to decreased pericyte loss and vascular leakage compared with control. CONCLUSIONS/

interpretationIntravitreal delivery of Ad-αAc-Gfp protects against vascular leakage in the streptozotocin-induced model of diabetes. This effect is associated with the inhibition of diabetic retinal pericyte loss in early diabetes, suggesting that αA-crystallin has a role in preventing the pathogenesis of early diabetic retinopathy.

Indexed as

Adenoviridaealpha-Crystallin A ChainAnimalsApoptosisCells, CulturedDiabetes Mellitus, ExperimentalDiabetic RetinopathyDisease Models, AnimalDrug Delivery SystemsGlucoseIntravitreal InjectionsMaleMiceMice, Inbred C57BLPericytesStreptozocinalpha-Crystallin A ChainGlucoseStreptozocin

Identifiers

PMID22772798
OpenAlexW2168304286

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.