Evidence map›Paper›PMID 33262633›Full record

ArticleJournal of inflammation research2020

Clusterin Deficiency Predisposes C57BL/6j Mice to Cationic Bovine Serum Albumin-Induced Glomerular Inflammation.

Pengcheng Sun, Shijian Feng, Qiunong Guan, Hans Adomat, Sean Barbour, Martin E Gleave, Christopher Y C Nguan, Wanhai Xu, Caigan Du

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of inflammation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
  5. 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

9 authors at 2 institutions in 2 countries.

Pengcheng SunDepartment of Urologic Sciences, University of British Columbia, Vancouver, BC V6H 3Z6, Canada.
Shijian FengDepartment of Urologic Sciences, University of British Columbia, Vancouver, BC V6H 3Z6, Canada.
Qiunong GuanDepartment of Urologic Sciences, University of British Columbia, Vancouver, BC V6H 3Z6, Canada.
Hans AdomatDepartment of Urologic Sciences, University of British Columbia, Vancouver, BC V6H 3Z6, Canada.
Sean BarbourDivision of Nephrology, Department of Medicine, University of British Columbia, Vancouver, BC V5T 3A5, Canada.
Martin E GleaveDepartment of Urologic Sciences, University of British Columbia, Vancouver, BC V6H 3Z6, Canada.
Christopher Y C NguanDepartment of Urologic Sciences, University of British Columbia, Vancouver, BC V6H 3Z6, Canada.
Wanhai XuHeilongjiang Key Laboratory of Scientific Research in Urology, Department of Urology, The Fourth Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, People's Republic of China.
Caigan DuDepartment of Urologic Sciences, University of British Columbia, Vancouver, BC V6H 3Z6, Canada.ORCID 0000-0001-8605-5501
University of British Columbia · CAHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMembranous nephropathy (MN) is a specific entity of glomerulonephritis, and its glomerular inflammation is characterized by the deposition of immune complexes in the glomerular basement membrane and proteinuria. However, the molecular mechanisms underlying the glomerular inflammation of MN are not fully understood. This study was designed to investigate the role of clusterin (CLU) in the development of MN using a mouse model of cationic bovine serum albumin (cBSA)-induced MN.

methodsBoth wild-type C57BL/6j (WT) and CLU-knockout C57BL/6j (CLU-KO) mice were immunized with cBSA. The kidney function was determined by the levels of serum creatinine (SCr), blood urea nitrogen (BUN) and urinary protein. MN and glomerular deposits of CLU, complement C3 and immunoglobulins (Igs) were determined by histological analyses. Serum proteins were analyzed by the enzyme-linked immunosorbent assay, Western blot and liquid chromatography-mass spectrometry.

resultsHere, we showed that after cBSA immunization, SCr and proteinuria were increased in CLU-KO mice but not in WT mice. Similarly, severe glomerular atrophy and mesangial expansion along with C3 deposit were only found in the kidneys of CLU-KO mice but not in WT mice. However, there were no differences of serum IgG and complement 3 levels between CLU-KO and WT mice. In the serum of WT mice, CLU bound to anti-cBSA IgG, complements (eg, C8), proteinase/protease inhibitors and antioxidative proteins to form a complex, and incubation with WT serum reduced the complement-dependent lysis of podocytes in cultures.

conclusionOur data suggest that a CLU deficiency induces cBSA-initiated glomerular inflammation of MN in a disease-resistant strain of mice, suggesting an anti-glomerular inflammatory function of CLU in the resistance to MN development. This function may be at least in part due to the formation of CLU-anti-cBSA Igs complex that prevents glomerular inflammation or injury in the disease-resistant mice.

Indexed as

glomerulonephritisimmune complexinflammatory glomerular diseasemembranous nephropathymouse model

Identifiers

PMID33262633
PMCPMC7699998
OpenAlexW3107459517

What Socratic holds

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LicenceCC BY-NC
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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 Socratic graph.