Evidence map›Paper›PMID 32120359›Full record

ArticleAnatolian journal of cardiology2020

Advanced glycation end products facilitate the proliferation and reduce early apoptosis of cardiac microvascular endothelial cells via PKCβ signaling pathway: Insight from diabetic cardiomyopathy.

Yi Luan, Jiefang Zhang, Min Wang, Guosheng Fu, Wenbin Zhang

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Anatolian journal of cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 32% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. 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 2 countries.

Yi LuanDepartment of Cardiology, Key Laboratory of Cardiovascular Intervention and Regenerative Medicine, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University; Zhejiang-P.R. China.
Jiefang ZhangDepartment of Cardiology, Key Laboratory of Cardiovascular Intervention and Regenerative Medicine, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University; Zhejiang-P.R. China.
Min WangDepartment of Cardiology, Key Laboratory of Cardiovascular Intervention and Regenerative Medicine, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University; Zhejiang-P.R. China.
Guosheng FuDepartment of Cardiology, Key Laboratory of Cardiovascular Intervention and Regenerative Medicine, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University; Zhejiang-P.R. China.
Wenbin ZhangDepartment of Cardiology, Key Laboratory of Cardiovascular Intervention and Regenerative Medicine, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University; Zhejiang-P.R. China.
Sir Run Run Shaw Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the effects of advanced glycation end products (AGEs) on the proliferation and apoptosis of cardiac microvascular endothelial cells (CMECs) in rats and their underlying signaling pathway.

methodsCMECs were isolated from Sprague-Dawley rats. We first examined the effects of AGEs on the proliferation and apoptosis of CMECs and then tested whether protein kinase C (PKC) β blockers could counteract the effects of AGEs. The PKC agonists phorbol 12-myristate 13-acetate (PMA) and PKCβ blockers were also used to verify whether PKC could act independently on CMECs. The receptor for AGEs (RAGE)-small interfering RNA (siRNA) transfection was used to verify the effect of AGEs on PKC. Following the above steps, we explained whether AGEs regulated the CMEC proliferation and early apoptosis through the PKCβ signaling pathway. Proliferation of CMECs was detected using the Cell Counting Kit-8 (CCK-8) assay, and early apoptosis was determined using the Annexin V- Fluorescein Isothiocyanate (FITC)/propidium iodide (PI) double staining. Expression of proliferation and apoptosis-related proteins and PKC phosphorylation were determined by western blotting analysis. Cell cycle distributions were assayed using a BD FACSCalibur cell-sorting system.

resultsAGEs facilitated the proliferation of CMECs, upregulated phosphorylated extracellular signal regulated kinase (p-ERK), and accelerated the entry of cells from G1 phase to the S+G2/M phase, which was consistent with the upregulated cyclin D1 by AGEs. AGEs inhibited early apoptosis of CMECs by increasing the expression of survivin and decreasing the expression of cleaved-caspase3. All these effects can be reversed by PKCβ1/2inhibitors. In addition, AGE upregulated the RAGE expression and phosphorylation of PKCβ1/2 in CMECs, while the inhibition of RAGE reversed the phosphorylation, as well as the effects of AGEs on proliferation and apoptosis in CMECs.

conclusionThe study indicated that AGEs facilitated the proliferation and reduced early apoptosis of CMECs via the PKCβ signaling pathway.

Indexed as

AnimalsApoptosisCell ProliferationDiabetic CardiomyopathiesDisease Models, AnimalEndothelial CellsGlycation End Products, AdvancedMaleProtein Kinase C betaRatsRats, Sprague-DawleySignal TransductionGlycation End Products, AdvancedProtein Kinase C beta

Identifiers

PMID32120359
PMCPMC7222633
OpenAlexW2987035676

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.