Evidence map›Paper›PMID 20729399›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2010

Kallistatin attenuates endothelial apoptosis through inhibition of oxidative stress and activation of Akt-eNOS signaling.

Bo Shen, Lin Gao, Yi-Te Hsu, Grant Bledsoe, Makato Hagiwara, Lee Chao, Julie Chao

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

46 citing papers in PubMed, 81 citations in OpenAlex.

  1. Kallistatin levels in HIV-infected patients and effects of statin therapy.Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals · 2017
    Trial
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  11. TRIM27 contributes to glomerular endothelial cell injury in lupus nephritis by mediating the FoxO1 signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  12. Genetic Susceptibility to Acute Kidney Injury.Journal of clinical medicine · 2021
    Review
  13. Article
  14. Diabetes-induced upregulation of kallistatin levels exacerbates diabetic nephropathy via RAS activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
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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 2 institutions in 1 country.

Bo ShenDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425-2211, USA.
Lin Gao
Yi-Te Hsu
Grant Bledsoe
Makato Hagiwara
Lee Chao
Julie Chao
Medical University of South Carolina · USCharleston Southern University · US

Funding

Regulation and Function of Tissue KallikreinR01HL029397 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CHAO, JULIE · 1986 to 2012
$3.9M
RENAL KALLIKREIN-BINDING PROTEIN IN HYPERTENSIONR01HL044083 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CHAO, JULIE · 1990 to 2008
$2.1M
MUSC FACIL EXPANSION &RENOV: SLE C06RR015455 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND, JOHN R · 2002 to 2002
$2.0M
NCRR NIH HHS C06 RR015455NCRR NIH HHS C06-RR-015455NHLBI NIH HHS HL-29397NHLBI NIH HHS HL-44083NHLBI NIH HHS R01 HL029397NHLBI NIH HHS R01 HL044083
6 · The paper itself

Abstract

Kallistatin is a regulator of vascular homeostasis capable of controlling a wide spectrum of biological actions in the cardiovascular and renal systems. We previously reported that kallistatin inhibited intracellular reactive oxygen species formation in cultured cardiac and renal cells. The present study was aimed to investigate the role and mechanisms of kallistatin in protection against oxidative stress-induced vascular injury and endothelial cell apoptosis. We found that kallistatin gene delivery significantly attenuated aortic superoxide formation and glomerular capillary loss in hypertensive DOCA-salt rats. In cultured endothelial cells, kallistatin suppressed TNF-α-induced cellular apoptosis, and the effect was blocked by the pharmacological inhibition of phosphatidylinositol 3-kinase and nitric oxide synthase (NOS) and by the knockdown of endothelial NOS (eNOS) expression. The transduction of endothelial cells with adenovirus expressing dominant-negative Akt abolished the protective effect of kallistatin on endothelial apoptosis and caspase activity. In addition, kallistatin inhibited TNF-α-induced reactive oxygen species formation and NADPH oxidase activity, and these effects were attenuated by phosphatidylinositol 3-kinase and NOS inhibition. Kallistatin also prevented the induction of Bim protein and mRNA expression by oxidative stress. Moreover, the downregulation of forkhead box O 1 (FOXO1) and Bim expression suppressed TNF-α-mediated endothelial cell death. Furthermore, the antiapoptotic actions of kallistatin were accompanied by Akt-mediated FOXO1 and eNOS phosphorylation, as well as increased NOS activity. These findings indicate a novel role of kallistatin in the protection against vascular injury and oxidative stress-induced endothelial apoptosis via the activation of Akt-dependent eNOS signaling.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11Endothelium, VascularForkhead Box Protein O1Forkhead Transcription FactorsMaleMembrane ProteinsModels, AnimalNADPNerve Tissue ProteinsNitric OxideNitric Oxide Synthase Type IIIOxidative StressProto-Oncogene ProteinsApoptosis Regulatory ProteinsBcl2l11 protein, ratBcl-2-Like Protein 11Forkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, ratkallistatinMembrane ProteinsNADPNerve Tissue ProteinsNitric OxideNitric Oxide Synthase Type IIIProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSerpinsTumor Necrosis Factor-alpha

Identifiers

PMID20729399
PMCPMC2993212
OpenAlexW2156879778

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.