Evidence map›Paper›PMID 16294224›Full record

ArticleThe Journal of clinical investigation2005

Identification of thrombospondin 1 (TSP-1) as a novel mediator of cell injury in kidney ischemia.

Charuhas V Thakar, Kamyar Zahedi, Monica P Revelo, Zhaohui Wang, Charles E Burnham, Sharon Barone, Shannon Bevans, Alex B Lentsch, Hamid Rabb, Manoocher Soleimani

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.

  1. Pooled it
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  18. Thrombospondin-1 in maladaptive aging responses: a concept whose time has come.American journal of physiology. Cell physiology · 2020
    Review
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  20. Article

6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Charuhas V ThakarDepartment of Medicine, University of Cincinnati School of Medicine, Cincinnati, Ohio 45267-0585, USA.
Kamyar Zahedi
Monica P Revelo
Zhaohui Wang
Charles E Burnham
Sharon Barone
Shannon Bevans
Alex B Lentsch
Hamid Rabb
Manoocher Soleimani
University of Cincinnati · US

Funding

REGULATION OF HEPATIC ISCHEMIA/REPERFUSION INJURYR01DK056029 · NIDDK · UNIVERSITY OF LOUISVILLE · PI LENTSCH, ALEX B. · 2000 to 2018
$6.0M
T Cell Modulation of Renal Ischemia Reperfusion InjuryR01DK054770 · NIDDK · MINNEAPOLIS MEDICAL RESEARCH FDN, INC. · PI RABB, HAMID · 2000 to 2009
$3.2M
Polyamine metabolism in heart and kidney ischemic injuryR21DK066589 · NIDDK · UNIVERSITY OF CINCINNATI · PI SOLEIMANI, MANOOCHER · 2004 to 2005
$307k
NIDDK NIH HHS DK 54770NIDDK NIH HHS DK 66589NIDDK NIH HHS R01 DK054770NIDDK NIH HHS R01 DK056029NIDDK NIH HHS R21 DK066589
6 · The paper itself

Abstract

Thrombospondin 1 (TSP-1) is a matricellular protein that inhibits angiogenesis and causes apoptosis in vivo and in vitro in several cancerous cells and tissues. Here we identify TSP-1 as the molecule with the highest induction level at 3 hours of IR injury in rat and mouse kidneys subjected to ischemia/reperfusion (IR) injury using the DNA microarray approach. Northern hybridizations demonstrated that TSP-1 expression was undetectable at baseline, induced at 3 and 12 hours, and returned to baseline levels at 48 hours of reperfusion. Immunocytochemical staining identified the injured proximal tubules as the predominant sites of expression of TSP-1 in IR injury and showed colocalization of TSP-1 with activated caspase-3. Addition of purified TSP-1 to normal kidney proximal tubule cells or cells subjected to ATP depletion in vitro induced injury as demonstrated by cytochrome c immunocytochemical staining and caspase-3 activity. The deleterious role of TSP-1 in ischemic kidney injury was demonstrated directly in TSP-1 null mice, which showed significant protection against IR injury-induced renal failure and tubular damage. We propose that TSP-1 is a novel regulator of ischemic damage in the kidney and may play an important role in the pathophysiology of ischemic kidney failure.

Indexed as

Adenosine TriphosphateAnimalsBinding SitesBlotting, NorthernBlotting, WesternCaspase 3CaspasesCD36 AntigensColorimetryCytochromes cDNA, ComplementaryEnzyme ActivationGene DeletionImmunoblottingImmunohistochemistryIn Situ Nick-End LabelingAdenosine TriphosphateCasp3 protein, mouseCasp3 protein, ratCaspase 3CaspasesCD36 AntigensCytochromes cDNA, ComplementaryRNARNA, MessengerThrombospondin 1

Identifiers

PMID16294224
PMCPMC1283940
OpenAlexW2127802406

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.