Evidence map›Paper›PMID 16545694›Full record

ArticleFree radical biology & medicine2006

Effect of heme and heme oxygenase-1 on vascular endothelial growth factor synthesis and angiogenic potency of human keratinocytes.

Agnieszka Jazwa, Agnieszka Loboda, Slawomir Golda, Jaroslaw Cisowski, Magdalena Szelag, Anna Zagorska, Patrycja Sroczynska, Justyna Drukala, Alicja Jozkowicz, Jozef Dulak

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In one paragraph

Article in Free radical biology & medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 89 citations in OpenAlex.

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  11. The Role of miR-378a in Metabolism, Angiogenesis, and Muscle Biology.International journal of endocrinology · 2015
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  18. Increased levels of plasma haemoxygenase-1 in prostate cancer.Prostate cancer and prostatic diseases · 2011
    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

10 authors at 1 institution in 1 country.

Agnieszka JazwaDepartment of Medical Biotechnology, Faculty of Biotechnology, Jagiellonian University, Gronostajowa 7, 30-387 Krakow, Poland.
Agnieszka Loboda
Slawomir Golda
Jaroslaw Cisowski
Magdalena Szelag
Anna Zagorska
Patrycja Sroczynska
Justyna Drukala
Alicja Jozkowicz
Jozef Dulak
Jagiellonian University · PL

Funding

Wellcome Trust 073974
6 · The paper itself

Abstract

backgroundSkin injury leads to the release of heme, a potent prooxidant which is degraded by heme oxygenase-1 (HO-1) to carbon monoxide, iron, and biliverdin, subsequently reduced to bilirubin. Recently the involvement of HO-1 in angiogenesis has been shown; however, the role of heme and HO-1 in wound healing angiogenesis has not been yet investigated.

resultsTreatment of HaCaT keratinocytes with hemin (heme chloride) induced HO-1 expression and activity. The effect of heme on vascular endothelial growth factor (VEGF) synthesis is variable: induction is significant after a short, 6 h treatment with heme, while longer stimulation may attenuate its production. The involvement of HO-1 in VEGF synthesis was confirmed by inhibition of VEGF expression by SnPPIX, a blocker of HO activity and by attenuation of HO-1 mRNA expression with specific siRNA. Importantly, induction of HO-1 by hemin was able to overcome the inhibitory effect of high glucose on VEGF synthesis. Moreover, HO-1 expression was also induced in keratinocytes cultured in hypoxia, with concomitant augmentation of VEGF production, which was further potentiated by hemin stimulation. Accordingly, conditioned media from keratinocytes overexpressing HO-1 enhanced endothelial cell proliferation and augmented formation of capillaries in angiogenic assay in vitro.

conclusionsHO-1 is involved in hemin-induced VEGF expression in HaCaT and may play a role in hypoxic regulation of this protein. HO-1 overexpression may be beneficial in restoring the proper synthesis of VEGF disturbed in diabetic conditions.

Indexed as

Cell ProliferationCells, CulturedCulture Media, ConditionedEndothelium, VascularFree RadicalsGlucoseHeme Oxygenase-1HeminHumansHypoxiaKeratinocytesNeovascularization, PhysiologicPromoter Regions, GeneticRNA, Small InterferingVascular Endothelial Growth Factor AWound HealingCulture Media, ConditionedFree RadicalsGlucoseHeme Oxygenase-1HeminRNA, Small InterferingVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID16545694
PMCPMC1414644
OpenAlexW2037686094

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Registered trials

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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.