Evidence map›Paper›PMID 19158958›Full record

ArticleMolecular vision2009

Apoptosis induction by oxidized glycated LDL in human retinal capillary pericytes is independent of activation of MAPK signaling pathways.

J Matthew Diffley, Mingyuan Wu, Mimi Sohn, Weiwei Song, Samar M Hammad, Timothy J Lyons

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.5field-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

23 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Salidroside Reduces High-Glucose-Induced Podocyte Apoptosis and Oxidative Stress via Upregulating Heme Oxygenase-1 (HO-1) Expression.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Modified Lipoproteins in Diabetic Retinopathy: A Local Action in the Retina.Journal of clinical & experimental ophthalmology · 2013
    Article
  14. Article
  15. Article
  16. Article
  17. Article
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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 1 institution in 1 country.

J Matthew DiffleyHarold Hamm Oklahoma Diabetes Center and Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
Mingyuan Wu
Mimi Sohn
Weiwei Song
Samar M Hammad
Timothy J Lyons
University of Oklahoma Health Sciences Center · US

Funding

Trt. of Primary Hyperaldosteronism w/ACE Inhibitors &Angiotension Rec. BlockersM01RR014467 · NCRR · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI TUCKER, PHEBE M · 2001 to 2007
$10.4M
NCRR NIH HHS M01 RR014467NCRR NIH HHS M01 RR-14467
6 · The paper itself

Abstract

backgroundPericyte loss is a cardinal feature of early diabetic retinopathy. We previously reported that highly oxidized-glycated low density lipoprotein (HOG-LDL) induces pericyte apoptosis in vitro. In this study, we investigated the role of the mitogen-activated protein kinase (MAPK) signaling pathways in HOG-LDL-induced apoptosis in human pericytes.

methodsHuman retinal capillary pericytes (HRCP) were exposed to native LDL (N-LDL) and HOG-LDL, and apoptosis was measured using flow cytometry. Time- and dose-dependent responses of extracellular signal-regulated kinase (ERK), p38, and Jun N-terminal kinase (JNK) following exposure to N-LDL or HOG-LDL were determined using western blotting. U0126 (ERK inhibitor), SB203580 (p38 inhibitor), and SP600125 (JNK inhibitor) were used to determine the role of MAPK signaling in HOG-LDL-induced apoptosis.

resultsHOG-LDL induced apoptosis in HRCP in a dose-dependent manner at concentrations from 5 to 50 mg/l, with a constant effect from 50 to 200 mg/l. When compared to serum-free medium (SFM), this effect of HOG-LDL was found to be significant at all doses above 10 mg/l. In contrast, N-LDL at 200 mg/l did not induce apoptosis compared with SFM. Exposure to N-LDL versus HOG-LDL induced similar phosphorylation of ERK, p38, and JNK, peaking at 5 min, with similar dose-dependent responses up to 25 mg/l that were constant from 25 to 100 mg/l. Blocking of the ERK, p38, and JNK pathways did not inhibit pericyte apoptosis induced by HOG-LDL.

conclusionsOur data suggest that apoptosis induced by HOG-LDL in HRCP is independent of the activation of MAPK signaling pathways.

Indexed as

AnthracenesApoptosisButadienesCapillariesExtracellular Signal-Regulated MAP KinasesGlycated ProteinsGlycation End Products, AdvancedHumansImidazolesJNK Mitogen-Activated Protein KinasesLipoproteins, LDLMAP Kinase Signaling SystemNitrilesp38 Mitogen-Activated Protein KinasesPericytesPhosphorylationAnthracenesButadienesExtracellular Signal-Regulated MAP Kinasesglycated lipoproteins, LDLGlycated ProteinsGlycation End Products, AdvancedImidazolesJNK Mitogen-Activated Protein KinasesLipoproteins, LDLNitrilesoxidized low density lipoproteinp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorspyrazolanthronePyridinesSB 203580U 0126

Identifiers

PMID19158958
PMCPMC2628314
OpenAlexW2111489239

What OpenQuestion holds

Textmetadata
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.