Evidence map›Paper›PMID 22796763›Full record

ArticleActa pharmacologica Sinica2012

Calcium mediates high glucose-induced HIF-1α and VEGF expression in cultured rat retinal Müller cells through CaMKII-CREB pathway.

Jun Li, Shu-zhi Zhao, Pei-pei Wang, Song-ping Yu, Zhi Zheng, Xun Xu

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  9. Article
  10. Research progress on the role of CaMKII in heart disease.American journal of translational research · 2020
    Review
  11. Article
  12. Article
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  15. Article
  16. Article
  17. High Glucose and Glucose Deprivation Modulate Müller Cell Viability and VEGF Secretion.International journal of ophthalmology & eye science · 2016
    Article
  18. Autophagy in Diabetic Retinopathy.Current neuropharmacology · 2016
    Review
  19. Article
  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

6 authors at 3 institutions in 1 country.

Jun LiDepartment of Ophthalmology, Shanghai First People's Hospital Affiliated Shanghai Jiao Tong University, Shanghai 200080, China.
Shu-zhi Zhao
Pei-pei Wang
Song-ping Yu
Zhi Zheng
Xun Xu
Lishui City People's Hospital · CNShanghai Jiao Tong University · CNShanghai First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo investigate the effects of high glucose (HG) medium on expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in cultured rat retinal Müller cells and to determine the signaling pathways mediating the effects.

methodsPrimary cultures of retinal Müller cells were prepared from Sprague-Dawley rats, and incubated in a medium containg HG (30 mmol/L) in the presence of the membrane-permeable Ca(2+) chelator BAPTA-AM (10 μmol/L) or the CaMKII inhibitor KN93 (10 μmol/L). The levels of CaMKII, p-CaMKII, CREB, p-CREB, HIF-1α, and VEGF proteins were measured with Western blotting, while HIF-1á and VEGF mRNA levels were determined using real-time RT-PCR.

resultsThe stimulation of retinal Müller cell with HG for 24 h remarkably increased the expression levels of HIF-1α and VEGF. These responses were significantly inhibited in the presence of BAPTA-AM or KN93. Both BAPTA-AM and KN93 also significantly inhibited HG-induced phosphorylation of CaMKII and CREB in the cultured retinal Müller cells. Transfection of the cultured retinal Müller cells with antisense CREB oligonucleotide (300 nmol/L) was similarly effective in blocking the HG-induced increase of HIF-1α and VEGF.

conclusionHG-induced HIF-1α and VEGF expression in cultured rat retinal Müller cells depends on intracellular free Ca(2+) and activation of CaMKII-CREB pathway. The activation of CaMKII-CREB pathway by HG may be a possible mechanism underlying the pathogenesis of diabetic retinopathy.

Indexed as

AnimalsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Chelating AgentsCells, CulturedCyclic AMP Response Element-Binding ProteinEpendymoglial CellsGene Expression RegulationGlucoseHypoxia-Inducible Factor 1, alpha SubunitRatsRats, Sprague-DawleySignal TransductionVascular Endothelial Growth Factor ACalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Chelating AgentsCyclic AMP Response Element-Binding ProteinGlucoseHif1a protein, ratHypoxia-Inducible Factor 1, alpha SubunitVascular Endothelial Growth Factor Avascular endothelial growth factor A, rat

Identifiers

PMID22796763
PMCPMC4011316
OpenAlexW2008479646

What OpenQuestion holds

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Registered trials

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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.