Evidence map›Paper›PMID 18464929›Full record

ArticleThe Journal of clinical investigation2008

p21Cip1 modulates arterial wound repair through the stromal cell-derived factor-1/CXCR4 axis in mice.

Michelle Olive, Jason A Mellad, Leilani E Beltran, Mingchao Ma, Thomas Cimato, Audrey C Noguchi, Hong San, Richard Childs, Jason C Kovacic, Manfred Boehm

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.2field-weighted citation impact, top 13% 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, 59 citations in OpenAlex.

  1. Article
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  3. Mast cell activation and degranulation in acute artery injury: A target for post-operative therapy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
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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

10 authors at 2 institutions in 1 country.

Michelle OliveGenome Technology Branch, National Human Genome Research Institute, Bethesda, Maryland 20817, USA.
Jason A Mellad
Leilani E Beltran
Mingchao Ma
Thomas Cimato
Audrey C Noguchi
Hong San
Richard Childs
Jason C Kovacic
Manfred Boehm
National Heart Lung and Blood Institute · USNational Human Genome Research Institute · US

Funding

Allogeneic Immunotherapy for cancer and nonmalignant hematological disordersZIAHL002345 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CHILDS, RICHARD · 2009 to 2025
$53.3M
Light Microscopy CoreZICHL006019 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI COMBS, CHRISTIAN · 2009 to 2025
$29.3M
Allogeneic Immunotherapy for cancer and nonmalignant hematological disordersZ01HL002345 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CHILDS, RICHARD · 2000 to 2008
$6.5M
Stem cell biology in cardiovascular regenerationZ01HL005066 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI BOEHM, MANFRED · 2004 to 2008
$4.6M
Stem cell biology in cardiovascular regenerationZIAHL005066 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI BOEHM, MANFRED · 2009 to 2009
$2.1M
Intramural NIH HHS
6 · The paper itself

Abstract

Cyclin-dependent kinase inhibitors, including p21Cip1, are implicated in cell turnover and are active players in cardiovascular wound repair. Here, we show that p21Cip1 orchestrates the complex interactions between local vascular and circulating immune cells during vascular wound repair. In response to femoral artery mechanical injury, mice with homozygous deletion of p21Cip1 displayed accelerated proliferation of VSMCs and increased immune cell infiltration. BM transplantation experiments indicated that local p21Cip1 plays a pivotal role in restraining excessive proliferation during vascular wound repair. Increased local vascular stromal cell-derived factor-1 (SDF-1) levels were observed after femoral artery injury in p21+/+ and p21-/- mice, although this was significantly greater in p21-/- animals. In addition, disruption of SDF-1/CXCR4 signaling inhibited the proliferative response during vascular remodeling in both p21+/+ and p21-/- mice. We provide evidence that the JAK/STAT signaling pathway is an important regulator of vascular SDF-1 levels and that p21Cip1 inhibits STAT3 binding to the STAT-binding site within the murine SDF-1 promoter. Collectively, these results suggest that p21Cip1 activity is essential for the regulation of cell proliferation and inflammation after arterial injury in local vascular cells and that the SDF-1/CXCR4 signaling system is a key mediator of vascular proliferation in response to injury.

Indexed as

ApoptosisWound HealingAnimalsCell ProliferationChemokine CXCL12Cyclin-Dependent Kinase Inhibitor p21Femoral ArteryHomozygoteMiceMice, TransgenicModels, BiologicalReceptors, CXCR4Time FactorsT-LymphocytesTumor Suppressor Protein p53Cdkn1a protein, mouseChemokine CXCL12Cyclin-Dependent Kinase Inhibitor p21Receptors, CXCR4Tumor Suppressor Protein p53

Identifiers

PMID18464929
PMCPMC2373418
OpenAlexW2037557338

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.