Evidence map›Paper›PMID 31133737›Full record

ArticleScientific reports2019

Possible role of complement factor H in podocytes in clearing glomerular subendothelial immune complex deposits.

Takeshi Zoshima, Satoshi Hara, Masakazu Yamagishi, Ira Pastan, Taiji Matsusaka, Mitsuhiro Kawano, Michio Nagata

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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 17 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

7 authors at 4 institutions in 2 countries.

Takeshi ZoshimaDivision of Rheumatology, Department of Internal Medicine, Kanazawa University Graduate School of Medicine, Takara-machi 13-1, Kanazawa, Ishikawa, 920-8640, Japan.
Satoshi HaraDivision of Rheumatology, Department of Internal Medicine, Kanazawa University Graduate School of Medicine, Takara-machi 13-1, Kanazawa, Ishikawa, 920-8640, Japan. satoshihara@staff.kanazawa-u.ac.jp.
Masakazu YamagishiDepartment of Cardiovascular and Internal Medicine, Kanazawa University Graduate School of Medicine, Takara-machi 13-1, Kanazawa, Ishikawa, 920-8640, Japan.ORCID http://orcid.org/0000-0003-4201-5094
Ira PastanLaboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, NIH, 37 Convent Dr, Room 5106, Bethesda, Maryland, 20892-4264, USA.ORCID http://orcid.org/0000-0002-9223-0270
Taiji MatsusakaDepartment of Molecular Life Sciences, Tokai University School of Medicine, Shimokasuya 143, Isehara, Kanagawa, 259-1193, Japan.
Mitsuhiro KawanoDivision of Rheumatology, Department of Internal Medicine, Kanazawa University Graduate School of Medicine, Takara-machi 13-1, Kanazawa, Ishikawa, 920-8640, Japan.
Michio NagataKidney and Vascular Pathology, Faculty of Medicine, University of Tsukuba, 1-1-1, Ten-nodai, Tsukuba, Ibaraki, 305-8577, Japan.
Kanazawa University · JPNational Cancer Institute · USTokai University · JPUniversity of Tsukuba · JP

Funding

Growth Regulation SectionZIABC010298 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI PASTAN, IRA · 2009 to 2023
$5.0M
6 · The paper itself

Abstract

Podocytes are known to express various complement factors including complement factor H (CFH) and to promote the removal of both subendothelial and subepithelial immune complex (IC) deposits. Using podocyte-selective injury model NEP25 mice and an IgG3-producing hybridoma clone 2B11.3 established by MRL/lpr mice, the present study investigated the role of podocyte complement regulation in only subendothelial IC deposition. In immunotoxin (LMB2) induced fatal podocyte injury (NEP25/LMB2) at day 12, glomerular CFH and C3a receptor (C3aR) expression was decreased as compared with NEP25/vehicle mice. In contrast, in sublytic podocyte injury 5 days after LMB2, glomerular CFH and C3aR expression was increased as compared with NEP25/vehicle mice. Intra-abdominal injection of 2B11.3 hybridoma to NEP25 mice (NEP25/hybridoma) caused IC deposition limited to the subendothelial area associated with unaltered CFH expression. NEP25/hybridoma mice with sublytic podocyte injury (NEP25/hybridoma/LMB2) resulted in increased glomerular CFH expression (1.7-fold) accompanied by decreased subendothelial IC deposition, as compared with NEP25/hybridoma. Immunostaining revealed that CFH was dominantly expressed in podocytes of NEP25/hybridoma/LMB2. In addition, puromycin-induced sublytic podocyte injury promoted CFH expression in immortalized mouse podocytes in vitro. These results suggest that in response to sublytic levels of injury, podocyte induced CFH expression locally and clearance of subendothelial IC deposits.

Indexed as

AnimalsAntigen-Antibody ComplexCell LineComplement Factor HComplement System ProteinsKidney GlomerulusMicePodocytesAntigen-Antibody ComplexComplement Factor HComplement System Proteins

Identifiers

PMID31133737
PMCPMC6536504
OpenAlexW2945787030

What OpenQuestion holds

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LicenceCC BY
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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.