Evidence map›Paper›PMID 18554097›Full record

ArticleHuman gene therapy2008

Kallikrein-modified mesenchymal stem cell implantation provides enhanced protection against acute ischemic kidney injury by inhibiting apoptosis and inflammation.

Makoto Hagiwara, Bo Shen, Lee Chao, Julie Chao

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

Article in Human gene therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 104 citations in OpenAlex.

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  18. Extracellular vesicles from bone marrow-derived mesenchymal stem cells protect against murine hepatic ischemia/reperfusion injury.Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society · 2017
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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

4 authors at 1 institution in 1 country.

Makoto HagiwaraDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA.
Bo Shen
Lee Chao
Julie Chao
Medical University of South Carolina · US

Funding

Regulation and Function of Tissue KallikreinR01HL029397 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CHAO, JULIE · 1986 to 2012
$3.9M
MUSC FACIL EXPANSION &RENOV: SLE C06RR015455 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND, JOHN R · 2002 to 2002
$2.0M
Tissue Kallikrein, Oxidative Stress and Renal FibrosisR01DK066350 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CHAO, JULIE · 2004 to 2007
$1.1M
NCRR NIH HHS C60 RR015455NHLBI NIH HHS HL-29397NHLBI NIH HHS R01 HL029397NIDDK NIH HHS DK-066350NIDDK NIH HHS R01 DK066350
6 · The paper itself

Abstract

Mesenchymal stem cells (MSCs) migrate to sites of tissue injury and serve as an ideal vehicle for cellular gene transfer. As tissue kallikrein has pleiotropic effects in protection against oxidative organ damage, we investigated the potential of kallikrein-modified MSCs (TK-MSCs) in healing injured kidney after acute ischemia/reperfusion (I/R). TK-MSCs secreted recombinant human kallikrein with elevated vascular endothelial growth factor levels in culture medium, and were more resistant to oxidative stress-induced apoptosis than control MSCs. Expression of human kallikrein was identified in rat glomeruli after I/R injury and systemic TK-MSC injection. Engrafted TK-MSCs exhibited advanced protection against renal injury by reducing blood urea nitrogen, serum creatinine levels, and tubular injury. Six hours after I/R, TK-MSC implantation significantly reduced renal cell apoptosis in association with decreased inducible nitric oxide synthase expression and nitric oxide levels. Forty-eight hours after I/R, TK-MSCs inhibited interstitial neutrophil and monocyte/macrophage infiltration and decreased myeloperoxidase activity, superoxide formation, p38 mitogen-activated protein kinase phosphorylation, and expression of tumor necrosis factor-alpha, monocyte chemoattractant protein-1, and intercellular adhesion molecule-1. In addition, tissue kallikrein and kinin significantly inhibited H2O2-induced apoptosis and increased Akt phosphorylation and cell viability in cultured proximal tubular cells. These results indicate that implantation of kallikrein-modified MSCs in the kidney provides advanced benefits in protection against ischemia-induced kidney injury by suppression of apoptosis and inflammation.

Indexed as

ApoptosisMesenchymal Stem Cell TransplantationAnimalsGene ExpressionGene Transfer TechniquesHumansHydrogen PeroxideInflammationKidneyKininsMaleMesenchymal Stem CellsNitric OxideNitric Oxide Synthase Type IIOxidative StressRatsHydrogen PeroxideKininsNitric OxideNitric Oxide Synthase Type IINOS2 protein, humanReactive Oxygen SpeciesRecombinant ProteinsTissue Kallikreins

Identifiers

PMID18554097
PMCPMC2743018
OpenAlexW2069325081

What OpenQuestion holds

Textmetadata
LicenceTDM
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.