Evidence map›Paper›PMID 17360568›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

Impaired angiogenesis in aminopeptidase N-null mice.

Roberto Rangel, Yan Sun, Liliana Guzman-Rojas, Michael G Ozawa, Jessica Sun, Ricardo J Giordano, Carolyn S Van Pelt, Peggy T Tinkey, Richard R Behringer, Richard L Sidman and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

68 citing papers in PubMed, 127 citations in OpenAlex.

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8 more citing papers are in PubMed but not listed here.

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

12 authors at 4 institutions in 3 countries.

Roberto RangelDepartment of Genitourinary Medical Oncology, University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
Yan Sun
Liliana Guzman-Rojas
Michael G Ozawa
Jessica Sun
Ricardo J Giordano
Carolyn S Van Pelt
Peggy T Tinkey
Richard R Behringer
Richard L Sidman
Wadih Arap
Renata Pasqualini
Spanish Oncology Genitourinary Group · ESThe University of Texas MD Anderson Cancer Center · USBeth Israel Deaconess Medical Center · USCentre for Cancer Biology · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aminopeptidase N (APN, CD13; EC 3.4.11.2) is a transmembrane metalloprotease with several functions, depending on the cell type and tissue environment. In tumor vasculature, APN is overexpressed in the endothelium and promotes angiogenesis. However, there have been no reports of in vivo inactivation of the APN gene to validate these findings. Here we evaluated, by targeted disruption of the APN gene, whether APN participates in blood vessel formation and function under normal conditions. Surprisingly, APN-null mice developed with no gross or histological abnormalities. Standard neurological, cardiovascular, metabolic, locomotor, and hematological studies revealed no alterations. Nonetheless, in oxygen-induced retinopathy experiments, APN-deficient mice had a marked and dose-dependent deficiency of the expected retinal neovascularization. Moreover, gelfoams embedded with growth factors failed to induce functional blood vessel formation in APN-null mice. These findings establish that APN-null mice develop normally without physiological alterations and can undergo physiological angiogenesis but show a severely impaired angiogenic response under pathological conditions. Finally, in addition to vascular biology research, APN-null mice may be useful reagents in other medical fields such as malignant, cardiovascular, immunological, or infectious diseases.

Indexed as

Gene Expression Regulation, EnzymologicNeovascularization, PhysiologicAnimalsCD13 AntigensExonsFemaleGenotypeMaleMiceMice, KnockoutMice, TransgenicModels, GeneticPhenotypeRetinal DegenerationCD13 Antigens

Identifiers

PMID17360568
PMCPMC1815469
OpenAlexW2149396308

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.