Evidence map›Paper›PMID 32209589›Full record

ArticleJournal of the American Society of Nephrology : JASN2020

SerpinB2 Regulates Immune Response in Kidney Injury and Aging.

Payel Sen, Alexandra Helmke, Chieh Ming Liao, Inga Sörensen-Zender, Song Rong, Jan-Hinrich Bräsen, Anette Melk, Hermann Haller, Sibylle von Vietinghoff, Roland Schmitt

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

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  17. Epsin1-mediated exosomal sorting of Dll4 modulates the tubular-macrophage crosstalk in diabetic nephropathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
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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

10 authors at 1 institution in 1 country.

Payel SenDepartment of Nephrology and Hypertension, Medical School Hannover, Hannover, Germany.
Alexandra HelmkeDepartment of Nephrology and Hypertension, Medical School Hannover, Hannover, Germany.
Chieh Ming LiaoDepartment of Nephrology and Hypertension, Medical School Hannover, Hannover, Germany.
Inga Sörensen-ZenderDepartment of Nephrology and Hypertension, Medical School Hannover, Hannover, Germany.
Song RongDepartment of Nephrology and Hypertension, Medical School Hannover, Hannover, Germany.
Jan-Hinrich BräsenDepartment of Pathology, Medical School Hannover, Hannover, Germany.
Anette MelkDepartment of Pediatric Nephrology and Gastroenterology, Medical School Hannover, Hannover, Germany.
Hermann HallerDepartment of Nephrology and Hypertension, Medical School Hannover, Hannover, Germany.
Sibylle von VietinghoffDepartment of Nephrology and Hypertension, Medical School Hannover, Hannover, Germany.
Roland SchmittDepartment of Nephrology and Hypertension, Medical School Hannover, Hannover, Germany schmitt.roland@mh-hannover.de.
Medizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExpression of SerpinB2, a regulator of inflammatory processes, has been described in the context of macrophage activation and cellular senescence. Given that mechanisms for these processes interact and can shape kidney disease, it seems plausible that SerpinB2 might play a role in renal aging, injury, and repair.

methodsWe subjected SerpinB2 knockout mice to ischemia-reperfusion injury or unilateral ureteral obstruction. We performed phagocyte depletion to study SerpinB2's role beyond the effects of macrophages and transplanted bone marrow from knockout mice to wild-type mice and

resultsCultured senescent tubular cells, kidneys of aged mice, and renal stress models exhibited upregulation of SerpinB2 expression. Functionally, lack of SerpinB2 in aged knockout mice had no effect on the magnitude of senescence markers but associated with enhanced kidney damage and fibrosis. In stress models, inflammatory cell infiltration was initially lower in knockout mice but later increased, leading to an accumulation of significantly more macrophages. SerpinB2 knockout tubular cells showed significantly reduced expression of the chemokine CCL2. Macrophages from knockout mice exhibited reduced phagocytosis and enhanced migration. Macrophage depletion and bone marrow transplantation experiments validated the functional relevance of these cell type-specific functions of SerpinB2.

conclusionsSerpinB2 influences tubule-macrophage crosstalk by supporting tubular CCL2 expression and regulating macrophage phagocytosis and migration. In mice, SerpinB2 expression seems to be needed for coordination and timely resolution of inflammation, successful repair, and kidney homeostasis during aging. Implications of SerpinB2 in human kidney disease deserve further exploration.

Indexed as

Acute Kidney InjuryAgingAnimalsCell MovementCellular SenescenceChemokine CCL2Coculture TechniquesEnzyme InductionEpithelial CellsFibrosisHomeostasisKidneyKidney TubulesMacrophagesMaleMiceCcl2 protein, mouseChemokine CCL2Plasminogen Activator Inhibitor 2acute renal failureChronic inflammationchronic kidney diseaseinterstitial fibrosiskidney tubulemacrophages

Identifiers

PMID32209589
PMCPMC7217424
OpenAlexW3013426462

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.