Evidence map›Paper›PMID 24088896›Full record

ArticleAmerican journal of physiology. Cell physiology2013

Cyp1B1 expression promotes angiogenesis by suppressing NF-κB activity.

Tammy L Palenski, Zafer Gurel, Christine M Sorenson, Kurt D Hankenson, Nader Sheibani

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  13. Thrombospondin-2 spatiotemporal expression in skeletal fractures.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2021
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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

5 authors at 3 institutions in 1 country.

Tammy L PalenskiDepartment of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin;
Zafer Gurel
Christine M Sorenson
Kurt D Hankenson
Nader Sheibani
Smith-Kettlewell Eye Research Institute · USUniversity of Pennsylvania · USUniversity of Wisconsin–Madison · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Christian Capitini · 1985 to 2026
$142.6M
UW Vision Research Core - Administrative CoreP30EY016665 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI Donna M Peters · 2005 to 2026
$12.6M
Molecular & Environmental Toxicology Pre-& Postdoctoral Training ProgramT32ES007015 · NIEHS · UNIVERSITY OF WISCONSIN-MADISON · PI CHRISTOPHER A BRADFIELD · 1985 to 2026
$11.5M
Integrated Multidisciplinary Strategies for Detection of Diabetic RetinopathiesRC4EY021357 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI ASSADI, AMIR H, ASSADI-PORTER, FARIBA M · 2010 to 2010
$3.2M
CYP1B1 and Retinopathy of PrematurityR01EY018179 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI SHEIBANI, NADER · 2009 to 2010
$713k
CYP1B1, NF-kB , and Regulation of AngiogenesisF31EY021091 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI PALENSKI, TAMMY LYNN · 2010 to 2012
$86k
NCI NIH HHS P30 CA-014520NEI NIH HHS F31 EY-021091NEI NIH HHS P30 EY-016665NEI NIH HHS P30 EY016665NEI NIH HHS R01 EY-016995NEI NIH HHS R01 EY-018179NEI NIH HHS R01 EY018179NEI NIH HHS RC4 EY-021357NIEHS NIH HHS T32 ES-007015NIEHS NIH HHS T32 ES007015
6 · The paper itself

Abstract

Nuclear factor-κB (NF-κB) is a master regulator of genes that control a large number of cellular processes, including angiogenesis and inflammation. We recently demonstrated that cytochrome P-450 1B1 (Cyp1B1) deficiency in endothelial cells (EC) and pericytes (PC) results in increased oxidative stress, alterations in migration, attenuation of capillary morphogenesis, sustained activation of NF-κB, and increased expression of thrombospondin-2 (TSP2), an endogenous inhibitor of angiogenesis. On the basis of a growing body of evidence that phenethyl isothiocyanate (PEITC) and pyrrolidine dithiocarbamate (PDTC) function as antioxidants and suppressors of NF-κB activation, we investigated their potential ability to restore a normal phenotype in Cyp1B1-deficient (cyp1b1(-/-)) vascular cells. PEITC and PDTC inhibited NF-κB activity and expression in cyp1b1(-/-) EC and PC. We also observed restoration of migration and capillary morphogenesis of cyp1b1(-/-) EC and decreased cellular oxidative stress in cyp1b1(-/-) EC and PC without restoration to normal TSP2 levels. In addition, expression of a dominant-negative inhibitor κBα, a suppressor of NF-κB activation, decreased NF-κB activity without affecting TSP2 expression in these cells. In contrast, knockdown of TSP2 expression resulted in attenuation of NF-κB activity in cyp1b1(-/-) vascular cells. Furthermore, expression of TSP2 in wild-type (cyp1b1(+/+)) cells resulted in increased NF-κB activity. Together, our results demonstrate an important role for TSP2 in modulation of NF-κB activity and attenuation of angiogenesis. Thus Cyp1B1 expression in vascular cells plays an important role in the regulation of vascular homeostasis through modulation of the cellular reductive state, TSP2 expression, and NF-κB activation.

Indexed as

Gene Expression RegulationAnimalsAryl Hydrocarbon HydroxylasesCells, CulturedCytochrome P-450 CYP1B1Endothelium, VascularGene Knockdown TechniquesMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNeovascularization, PhysiologicNF-kappa BRetinaThrombospondin 2ThrombospondinsAryl Hydrocarbon HydroxylasesCyp1b1 protein, mouseCytochrome P-450 CYP1B1NF-kappa BThrombospondin 2Thrombospondinsangiogenesiscell migrationisothiocyanatesNF-κBoxidative stressthrombospondins

Identifiers

PMID24088896
PMCPMC3882387
OpenAlexW2166319914

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.