Evidence map›Paper›PMID 30446855›Full record

ArticleAngiogenesis2019

ADAM10 controls the differentiation of the coronary arterial endothelium.

Gregory Farber, Matthew M Parks, Nicole Lustgarten Guahmich, Yi Zhang, Sébastien Monette, Scott C Blanchard, Annarita Di Lorenzo, Carl P Blobel

Open access · greenAbstract read
In one paragraph

Article in Angiogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.0field-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

26 citing papers in PubMed, 40 citations in OpenAlex.

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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

8 authors at 2 institutions in 2 countries.

Gregory FarberDepartment of Physiology, Biophysics and Systems Biology, Weill Cornell Medicine, New York, NY, USA.
Matthew M ParksDepartment of Physiology, Biophysics and Systems Biology, Weill Cornell Medicine, New York, NY, USA.
Nicole Lustgarten GuahmichDepartment of Physiology, Biophysics and Systems Biology, Weill Cornell Medicine, New York, NY, USA.
Yi ZhangCenter for Vascular Biology, Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, USA.
Sébastien MonetteLaboratory of Comparative Pathology, Hospital for Special Surgery, Memorial Sloan Kettering Cancer Center, The Rockefeller University, Weill Cornell Medicine, New York, NY, USA.
Scott C BlanchardDepartment of Physiology, Biophysics and Systems Biology, Weill Cornell Medicine, New York, NY, USA.
Annarita Di LorenzoCenter for Vascular Biology, Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, USA.
Carl P BlobelDepartment of Physiology, Biophysics and Systems Biology, Weill Cornell Medicine, New York, NY, USA. blobelc@hss.edu.ORCID 0000-0001-5053-3137
Cornell University · USHospital for Special Surgery · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
iRhoms 1 and 2: Key regulators of ADAM17-dependent EGFR signalingR01GM064750 · NIGMS · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI BLOBEL, CARL PETER · 2002 to 2019
$6.1M
Endothelial Sphingolipid Synthesis and Tissue Inflammatory ResponseR01HL126913 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI DI LORENZO, ANNARITA · 2015 to 2023
$3.5M
A NOVEL ISCHEMIC STROKE MODEL TRIGGERED BY ENDOTHELIAL DYSFUNCTIONR21NS104512 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI DI LORENZO, ANNARITA · 2018 to 2019
$466k
American Heart Association 17PRE33380001NCI NIH HHS P30 CA008748NHLBI NIH HHS R01 HL126913NIGMS NIH HHS R01 GM064750NINDS NIH HHS R21 NS104512
6 · The paper itself

Abstract

The coronary vasculature is crucial for normal heart function, yet much remains to be learned about its development, especially the maturation of coronary arterial endothelium. Here, we show that endothelial inactivation of ADAM10, a key regulator of Notch signaling, leads to defects in coronary arterial differentiation, as evidenced by dysregulated genes related to Notch signaling and arterial identity. Moreover, transcriptome analysis indicated reduced EGFR signaling in A10ΔEC coronary endothelium. Further analysis revealed that A10ΔEC mice have enlarged dysfunctional hearts with abnormal myocardial compaction, and increased expression of venous and immature endothelium markers. These findings provide the first evidence for a potential role for endothelial ADAM10 in cardioprotective homeostatic EGFR signaling and implicate ADAM10/Notch signaling in coronary arterial cell specification, which is vital for normal heart development and function. The ADAM10/Notch signaling pathway thus emerges as a potential therapeutic target for improving the regenerative capacity and maturation of the coronary vasculature.

Indexed as

ADAM10 ProteinAmyloid Precursor Protein SecretasesAnimalsCell DifferentiationCoronary VesselsEndothelial CellsEndothelium, VascularFemaleHeartMaleMembrane ProteinsMiceMice, 129 StrainMice, Inbred C57BLMice, TransgenicReceptors, NotchADAM10 ProteinAdam10 protein, mouseAmyloid Precursor Protein SecretasesMembrane ProteinsReceptors, NotchADAM10 (a disintegrin and metalloprotease 10)Arterial differentiationCoronary vasculatureEndothelial CellsNotch

Identifiers

PMID30446855
PMCPMC6475616
OpenAlexW2901167659

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.