Evidence map›Paper›PMID 23568032›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2013

Lack of Cyp1b1 promotes the proliferative and migratory phenotype of perivascular supporting cells.

Tammy L Palenski, Christine M Sorenson, Colin R Jefcoate, Nader Sheibani

Open access · bronzeAbstract read
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing 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

41 citing papers in PubMed, 53 citations in OpenAlex.

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  19. 1,25(OH)FASEB bioAdvances · 2019
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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.

Tammy L PalenskiDepartment of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Christine M Sorenson
Colin R Jefcoate
Nader Sheibani
University of Wisconsin–Madison · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
UW Vision Research Core - Administrative CoreP30EY016665 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI ROBERT W NICKELLS · 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
PECAM-1 and Retinopathy of PrematurityR01EY016695 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI SHEIBANI, NADER · 2007 to 2011
$1.6M
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 CA014520NEI NIH HHS EY016995NEI NIH HHS EY018179NEI NIH HHS F31 EY021091NEI NIH HHS P30 EY016665NEI NIH HHS R01 EY016695NEI NIH HHS R01 EY018179NEI NIH HHS RC4 EY021357NIEHS NIH HHS T32 ES007015
6 · The paper itself

Abstract

Perivascular supporting cells, including pericytes and smooth muscle cells (PC/SMC), have an integral role during angiogenesis and control vascular remodeling, maturation, and stabilization of neoteric vessels. We recently showed that a Cyp1B1 deficiency in mice results in the attenuation of angiogenesis in vivo and the pro-angiogenic activity of endothelial cells in vitro. However, the contribution of PC/SMC, and more specifically the cell autonomous effects of Cyp1B1 in these processes, needs further investigation. Here we demonstrate that PC constitutively expressed Cyp1B1, and that a deficiency in Cyp1B1 was associated with enhanced proliferation, and decreased apoptosis. Mechanistically, the lack of Cyp1B1 was associated with increased oxidative stress and sustained NF-κB activation, which was reversed by the antioxidant N-acetylcysteine. These changes were also concomitant with alterations in PC migration, adhesion, and expression of various extracellular matrix proteins, including thrombospondin-2. Cyp1B1-deficient PC also expressed decreased levels of vascular endothelial growth factor. Together, our results suggest an important role for Cyp1B1 expression in the regulation of PC proliferation, migration, and survival through modulation of the intracellular oxidative state and NF-κB expression and/or activity. Thus, a lack of Cyp1B1 in PC may have a significant role in vascular dysfunction and integrity, contributing to the attenuation of angiogenesis.

Indexed as

AnimalsApoptosisAryl Hydrocarbon HydroxylasesCell AdhesionCell MovementCell ProliferationCytochrome P-450 CYP1B1Extracellular Matrix ProteinsMiceMice, Inbred C57BLMice, TransgenicOxidative StressPericytesRetinal VesselsThrombospondin 2ThrombospondinsAryl Hydrocarbon HydroxylasesCyp1b1 protein, mouseCytochrome P-450 CYP1B1Extracellular Matrix ProteinsThrombospondin 2ThrombospondinsTranscription Factor RelAVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID23568032
PMCPMC3791926
OpenAlexW2088000560

What OpenQuestion holds

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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.