Evidence map›Paper›PMID 19246645›Full record

ArticleThe American journal of pathology2009

Anti-inflammatory and renal protective actions of stanniocalcin-1 in a model of anti-glomerular basement membrane glomerulonephritis.

Luping Huang, Gabriela Garcia, Yahuan Lou, Qin Zhou, Luan D Truong, Gabriel DiMattia, Xia Ru Lan, Hui Y Lan, Yanlin Wang, David Sheikh-Hamad

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 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

10 authors at 5 institutions in 4 countries.

Luping HuangBaylor College of Medicine, Nephrology Division, Department of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Gabriela Garcia
Yahuan Lou
Qin Zhou
Luan D Truong
Gabriel DiMattia
Xia Ru Lan
Hui Y Lan
Yanlin Wang
David Sheikh-Hamad
Baylor College of Medicine · USThe University of Texas Health Science Center at Houston · USUniversity of Hong Kong · HKCornell University · USLondon Cancer · GB

Funding

Renal Inflammation: Mechanisms and ConsequencesP50DK064233 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2003 to 2007
$5.1M
A Novel Type of Dendritic Cell in Prevention of GlomerulonephritisR01DK077857 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI LOU, YAHUAN · 2008 to 2015
$2.1M
SMAD SIGNALING IN ANGIOTENSIN II-MEDIATED RENAL FIBROSISR01DK062828 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2005 to 2006
$680k
NIDDK NIH HHS DK062828NIDDK NIH HHS DK62703-04NIDDK NIH HHS P50 DK064233NIDDK NIH HHS P50 DK64233-01NIDDK NIH HHS R01 DK062828NIDDK NIH HHS R01 DK077857
6 · The paper itself

Abstract

We have previously shown that stanniocalcin-1 (STC1) inhibits the transendothelial migration of macrophages and T cells, suppresses superoxide generation in macrophages, and attenuates macrophage responses to chemoattractants. To study the effects of STC1 on inflammation, in this study we induced a macrophage- and T-cell-mediated model of anti-glomerular basement membrane disease in STC1 transgenic mice, which display elevated serum STC1 levels and preferentially express STC1 in both endothelial cells and macrophages. We examined the following parameters both at baseline and after anti-glomerular basement membrane antibody treatment: blood pressure; C(3a) levels; urine output; proteinuria; blood urea nitrogen; and kidney C(3) deposition, fibrosis, histological changes, cytokine expression, and number of T cells and macrophages. Compared with wild-type mice, after anti-glomerular basement membrane treatment STC1 transgenic mice exhibited: i) diminished infiltration of inflammatory macrophages in the glomeruli; ii) marked reduction in crescent formation and sclerotic glomeruli; iii) decreased interstitial fibrosis; iv) preservation of kidney function and lower blood pressure; v) diminished C(3) deposition in the glomeruli; and vi) reduced expression of macrophage inhibitory protein-2 and transforming growth factor-beta2 in the kidney. Compared with baseline, wild-type mice, but not STC1 transgenic mice, had higher proteinuria and a marked reduction in urine output. STC1 had minimal effects, however, on both T-cell number in the glomeruli and interstitium and on cytokine expression characteristic of either TH1 or TH2 activation. These data suggest that STC1 is a potent anti-inflammatory and renal protective protein.

Indexed as

AnimalsAnti-Glomerular Basement Membrane DiseaseAutoantibodiesAutoantigensBlotting, WesternCytokinesDisease Models, AnimalGlomerular Basement MembraneGlycoproteinsImmunohistochemistryInflammationInflammation MediatorsKidney Function TestsMiceMice, Transgenicantiglomerular basement membrane antibodyAutoantibodiesAutoantigensCytokinesGlycoproteinsInflammation Mediatorsteleocalcin

Identifiers

PMID19246645
PMCPMC2671368
OpenAlexW1978748805

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.