Evidence map›Paper›PMID 25452119›Full record

ArticleThe American journal of pathology2015

Global deletion of Ankrd1 results in a wound-healing phenotype associated with dermal fibroblast dysfunction.

Susan E Samaras, Karinna Almodóvar-García, Nanjun Wu, Fang Yu, Jeffrey M Davidson

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

35 citing papers in PubMed, 50 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

5 authors at 1 institution in 1 country.

Susan E SamarasDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee.
Karinna Almodóvar-GarcíaDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee.
Nanjun WuDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee.
Fang YuDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee.
Jeffrey M DavidsonDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee; Research Service, Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee. Electronic address: jeff.davidson@vanderbilt.edu.
Vanderbilt University · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
Vanderbilt/Meharry Initiative for Minority Student DvptR25GM062459 · NIGMS · VANDERBILT UNIVERSITY · PI VELEZ EDWARDS, DIGNA R · 2002 to 2020
$10.4M
Skin Regeneration with Stem Cells and ScaffoldsR01AR056138 · NIAMS · VANDERBILT UNIVERSITY · PI DAVIDSON, JEFFREY M., GUELCHER, SCOTT A · 2009 to 2013
$3.3M
CARP: Angiogenic Gene Therapy in Diabetic WoundsR01DK065656 · NIDDK · VANDERBILT UNIVERSITY · PI DAVIDSON, JEFFREY M. · 2003 to 2011
$2.3M
Distinct roles of CARP target genes in wound healingF31GM101947 · NIGMS · VANDERBILT UNIVERSITY · PI ALMODOVAR, KARINNA · 2012 to 2013
$70k
NCI NIH HHS P30 CA068485NIAMS NIH HHS R01 AR056138NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P60 DK020593NIDDK NIH HHS R01 DK065656NIGMS NIH HHS F31 GM101947NIGMS NIH HHS R25 GM062459
6 · The paper itself

Abstract

The expression of ankyrin repeat domain protein 1 (Ankrd1), a transcriptional cofactor and sarcomeric component, is strongly elevated by wounding and tissue injury. We developed a conditional Ankrd1(fl/fl) mouse, performed global deletion with Sox2-cre, and assessed the role of this protein in cutaneous wound healing. Although global deletion of Ankrd1 did not affect mouse viability or development, Ankrd1(-/-) mice had at least two significant wound-healing phenotypes: extensive necrosis of ischemic skin flaps, which was reversed by adenoviral expression of ANKRD1, and delayed excisional wound closure, which was characterized by decreased contraction and reduced granulation tissue thickness. Skin fibroblasts isolated from Ankrd1(-/-) mice did not spread or migrate on collagen- or fibronectin-coated surfaces as efficiently as fibroblasts isolated from Ankrd1(fl/fl) mice. More important, Ankrd1(-/-) fibroblasts failed to contract three-dimensional floating collagen gels. Reconstitution of ANKRD1 by adenoviral infection stimulated both collagen gel contraction and actin fiber organization. These in vitro data were consistent with in vivo wound closure studies, and suggest that ANKRD1 is important for the proper interaction of fibroblasts with a compliant collagenous matrix both in vitro and in vivo.

Indexed as

Gene DeletionAdenoviridaeAnimalsCell MovementCollagenCrosses, GeneticExonsFemaleFibroblastsGelsGene Expression ProfilingGenotypeGreen Fluorescent ProteinsMaleMAP Kinase Signaling SystemMiceAnkrd1 protein, mouseCollagenGelsGreen Fluorescent ProteinsMuscle ProteinsNuclear ProteinsRepressor ProteinsRNA

Identifiers

PMID25452119
PMCPMC4278243
OpenAlexW1979581862

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.