Evidence map›Paper›PMID 31776394›Full record

ArticleScientific reports2019

Characterizing renal involvement in Hermansky-Pudlak Syndrome in a zebrafish model.

H Schenk, J Müller-Deile, P Schroder, P Bolaños-Palmieri, L Beverly-Staggs, R White, J H Bräsen, H Haller, M Schiffer

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 39% 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, 15 citations in OpenAlex.

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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

9 authors at 3 institutions in 2 countries.

H SchenkDepartment of Medicine/Nephrology, Hannover Medical School, 30625, Hannover, Germany. Schenk.Heiko@mh-hannover.de.ORCID http://orcid.org/0000-0003-2693-5712
J Müller-DeileDepartment of Medicine/Nephrology, Hannover Medical School, 30625, Hannover, Germany.
P SchroderMount Desert Island Biological Laboratory, Salisbury Cove, ME, 04672, USA.
P Bolaños-PalmieriDepartment of Medicine/Nephrology, Hannover Medical School, 30625, Hannover, Germany.
L Beverly-StaggsMount Desert Island Biological Laboratory, Salisbury Cove, ME, 04672, USA.
R WhiteMount Desert Island Biological Laboratory, Salisbury Cove, ME, 04672, USA.
J H BräsenInstitute of Pathology, Nephropathology Unit, Hannover Medical School, Hannover, Germany.
H HallerDepartment of Medicine/Nephrology, Hannover Medical School, 30625, Hannover, Germany.
M SchifferDepartment of Medicine/Nephrology, Hannover Medical School, 30625, Hannover, Germany. Mario.Schiffer@uk-erlangen.de.ORCID http://orcid.org/0000-0002-8414-1470
Mount Desert Island Biological Laboratory · USFriedrich-Alexander-Universität Erlangen-Nürnberg · DEMedizinische Hochschule Hannover · DE

Funding

The Maine Biomedical Research Network (INBRE)P20GM103423 · NIGMS · MOUNT DESERT ISLAND BIOLOGICAL LAB · PI Dustin Lynn Updike · 2012 to 2026
$60.0M
Understanding the role of thyroid hormone signaling during axolotl limb regenerationP20GM104318 · NIGMS · MOUNT DESERT ISLAND BIOLOGICAL LAB · PI DRUMMOND, IAIN A. · 2013 to 2023
$23.0M
NIGMS NIH HHS P20 GM103423NIGMS NIH HHS P20 GM104318
6 · The paper itself

Abstract

Hermansky-Pudlak Syndrome (HPS) is a rare disease caused by mutations in the genes coding for various HPS proteins. HPS proteins are part of multi-subunit complexes involved in the biogenesis of organelles from the lysosomal-endosomal-system. In humans, this syndrome is characterized by the presence of albinism, platelet dysfunction and pulmonary fibrosis. The renal component to the disease remains unstudied and untreated in patients with HPS. Here we demonstrate that in humans, HPS proteins have a high renal expression with active transcription of HPS1, 3, 4 and 5 in human podocyte cell culture, suggesting that impaired function of HPS proteins could directly impact renal function. Therefore, we developed a zebrafish model to study the renal involvement of HPS proteins in proteinuric kidney disease. Remarkably, knockdown of HPS genes in zebrafish causes glomerular injury with edema, proteinuria and structural changes of the glomerular filtration barrier. Moreover, reduced expression of HPS proteins in zebrafish recapitulates other important disease hallmarks, like hypopigmentation and accumulation of intracellular debris characteristic of lysosomal disorders. In conclusion, we present a valid zebrafish model that highlights the previously underestimated relevance of renal disease in HPS. This draws attention to the therapeutic options available to manage this component of the syndrome.

Indexed as

Disease Models, AnimalAnimalsCell LineCells, CulturedEndothelial CellsEndothelium, VascularHermanski-Pudlak SyndromeHumansKidneyLysosomesPodocytesZebrafishZebrafish ProteinsZebrafish Proteins

Identifiers

PMID31776394
PMCPMC6881439
OpenAlexW2990812709

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.