Evidence map›Paper›PMID 26447218›Full record

ArticleAmerican journal of physiology. Renal physiology2015

Mechanisms of bradykinin-induced expression of connective tissue growth factor and nephrin in podocytes.

J Abou Msallem, H Chalhoub, M Al-Hariri, L Saad, M A Jaffa, F N Ziyadeh, A A Jaffa

RetractedOpen access · greenAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 43% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 2 countries.

J Abou MsallemBiochemistry and Molecular Genetics Department, Faculty of Medicine, American University of Beirut, Beirut, Lebanon;
H ChalhoubBiochemistry and Molecular Genetics Department, Faculty of Medicine, American University of Beirut, Beirut, Lebanon;
M Al-HaririBiochemistry and Molecular Genetics Department, Faculty of Medicine, American University of Beirut, Beirut, Lebanon;
L SaadBiochemistry and Molecular Genetics Department, Faculty of Medicine, American University of Beirut, Beirut, Lebanon;
M A JaffaEpidemiology and Population Health Department, Faculty of Health Sciences, American University of Beirut, Beirut, Lebanon; and.
F N ZiyadehBiochemistry and Molecular Genetics Department, Faculty of Medicine, American University of Beirut, Beirut, Lebanon;
A A JaffaBiochemistry and Molecular Genetics Department, Faculty of Medicine, American University of Beirut, Beirut, Lebanon; Department of Medicine, Medical University of South Carolina, Charleston, South Carolina aj24@aub.edu.lb.
American University of Beirut · LB

Funding

MECHANISMS OF VASCULAR DISEASE IN DIABETESR01HL077192 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI JAFFA, AYAD A · 2006 to 2017
$3.4M
KALLIKREIN AND VASCULAR DISEASE RISK IN DIABETESR01HL087986 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI JAFFA, AYAD A · 2008 to 2011
$1.3M
NHLBI NIH HHS HL-077192NHLBI NIH HHS HL-087986
6 · The paper itself

Abstract

Diabetic nephropathy (DN) is the main cause of morbidity and mortality in diabetes and is characterized by mesangial matrix deposition and podocytopathy, including podocyte loss. The risk factors and mechanisms involved in the pathogenesis of DN are still not completely defined. In the present study, we aimed to understand the cellular mechanisms through which activation of B2 kinin receptors contribute to the initiation and progression of DN. Stimulation of cultured rat podocytes with bradykinin (BK) resulted in a significant increase in ROS generation, and this was associated with a significant increase in NADPH oxidase (NOX)1 and NOX4 protein and mRNA levels. BK stimulation also resulted in a signicant increase in the phosphorylation of ERK1/2 and Akt, and this effect was inhibited in the presence of NOX1 and Nox4 small interfering (si)RNA. Furthermore, podocytes stimulated with BK resulted in a significant increase in protein and mRNA levels of connective tissue growth factor (CTGF) and, at the same time, a significant decrease in protein and mRNA levels of nephrin. siRNA targeted against NOX1 and NOX4 significantly inhibited the BK-induced increase in CTGF. Nephrin expression was increased in response to BK in the presence of NOX1 and NOX4 siRNA, thus implicating a role for NOXs in modulating the BK response in podocytes. Moreover, nephrin expression in response to BK was also significantly increased in the presence of siRNA targeted against CTGF. These findings provide novel aspects of BK signal transduction pathways in pathogenesis of DN and identify novel targets for interventional strategies.

Indexed as

AnimalsBradykininCells, CulturedConnective Tissue Growth FactorDiabetic NephropathiesExtracellular Signal-Regulated MAP KinasesMembrane ProteinsNADH, NADPH OxidoreductasesNADPH Oxidase 1NADPH Oxidase 4NADPH OxidasesOxidative StressPhosphorylationPodocytesProto-Oncogene Proteins c-aktRatsBradykininCCN2 protein, ratConnective Tissue Growth FactorExtracellular Signal-Regulated MAP KinasesMembrane ProteinsNADH, NADPH OxidoreductasesNADPH Oxidase 1NADPH Oxidase 4NADPH OxidasesnephrinNOX1 protein, ratNox4 protein, ratProto-Oncogene Proteins c-aktReceptor, Bradykinin B2RNA, Messengerconnective tissue growth factordiabetic nephropathykinin receptorsnephrinoxidative stresspodocytes

Identifiers

PMID26447218
PMCPMC4669358
OpenAlexW2344237020

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.