Evidence map›Paper›PMID 32708451›Full record

ArticleCells2020

The Secretome Analysis of Activated Human Renal Fibroblasts Revealed Beneficial Effect of the Modulation of the Secreted Peptidyl-Prolyl Cis-Trans Isomerase A in Kidney Fibrosis.

Gry H Dihazi, Marwa Eltoweissy, Olaf Jahn, Björn Tampe, Michael Zeisberg, Hauke S Wülfrath, Gerhard A Müller, Hassan Dihazi

Abstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Mitochondrial fission inhibition protects against hypertension induced by angiotensin II.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Article
  4. Article
  5. Review
  6. 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

8 authors.

Gry H DihaziInstitute for Clinical Chemistry/UMG-Laboratories, University Medical Center Göttingen, Robert-Koch-Strasse 40, D-37075 Göttingen, Germany.
Marwa EltoweissyDepartment of Zoology, Faculty of Science, Alexandria University, Alexandria 21500, Egypt.
Olaf JahnProteomics Group, Max-Planck-Institute of Experimental Medicine, Hermann-Rein-Strasse 3, D-37075 Göttingen, Germany.ORCID 0000-0002-3397-8924
Björn TampeClinic for Nephrology and Rheumatology, University Medical Center Göttingen, Robert-Koch-Strasse 40, D-37075 Göttingen, Germany.
Michael ZeisbergClinic for Nephrology and Rheumatology, University Medical Center Göttingen, Robert-Koch-Strasse 40, D-37075 Göttingen, Germany.
Hauke S WülfrathInstitute for Clinical Chemistry/UMG-Laboratories, University Medical Center Göttingen, Robert-Koch-Strasse 40, D-37075 Göttingen, Germany.
Gerhard A MüllerClinic for Nephrology and Rheumatology, University Medical Center Göttingen, Robert-Koch-Strasse 40, D-37075 Göttingen, Germany.
Hassan DihaziClinic for Nephrology and Rheumatology, University Medical Center Göttingen, Robert-Koch-Strasse 40, D-37075 Göttingen, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The secretome is an important mediator in the permanent process of reciprocity between cells and their environment. Components of secretome are involved in a large number of physiological mechanisms including differentiation, migration, and extracellular matrix modulation. Alteration in secretome composition may therefore trigger cell transformation, inflammation, and diseases. In the kidney, aberrant protein secretion plays a central role in cell activation and transition and in promoting renal fibrosis onset and progression. Using comparative proteomic analyses, we investigated in the present study the impact of cell transition on renal fibroblast cells secretome. Human renal cell lines were stimulated with profibrotic hormones and cytokines, and alterations in secretome were investigated using proteomic approaches. We identified protein signatures specific for the fibrotic phenotype and investigated the impact of modeling secretome proteins on extra cellular matrix accumulation. The secretion of peptidyl-prolyl cis-trans isomerase A (PPIA) was demonstrated to be associated with fibrosis phenotype. We showed that the in-vitro inhibition of PPIA with ciclosporin A (CsA) resulted in downregulation of PPIA and fibronectin (FN1) expression and significantly reduced their secretion. Knockdown studies of PPIA in a three-dimensional (3D) cell culture model significantly impaired the secretion and accumulation of the extracellular matrix (ECM), suggesting a positive therapeutic effect on renal fibrosis progression.

Indexed as

Cell Line, TransformedCell SurvivalCyclosporineDisease ProgressionDown-RegulationExtracellular MatrixFibroblastsFibronectinsFibrosisHumansInflammationKidneyPeptidylprolyl IsomerasePhenotypeProteomeRNA, Small InterferingCyclosporineFibronectinsPeptidylprolyl IsomeraseProteomeRNA, Small InterferingTacrolimuskidney fibrosisPPIAsecretometransforming growth factor beta 1 (TGFβ1)

Identifiers

PMID32708451
PMCPMC7407823

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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.