Evidence map›Paper›PMID 21081489›Full record

ArticleThe Journal of biological chemistry2011

miR-200b targets Ets-1 and is down-regulated by hypoxia to induce angiogenic response of endothelial cells.

Yuk Cheung Chan, Savita Khanna, Sashwati Roy, Chandan K Sen

Registry-linked trialOpen access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02581098 (Novel Regulators of Wound Angiogenesis and Inflammation), which is not on this map. Cited by 130 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 3% 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.

NCT02581098 completednot on this mapstarted 2015, after this paper: background citation

Novel Regulators of Wound Angiogenesis and Inflammation

TypeobservationalSponsorIndiana UniversityRan2015 to 2023Enrolled98ConditionsDiabetes Mellitus, Foot Ulcer, Ulcer, Diabetic Foot UlcerArmsNo interventions
3 · Its place in the literature

Who cites it

130 citing papers in PubMed, 1 synthesis or guideline pooled it, 236 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Therapeutic Potential of Modulating Gene-MicroRNA Crosstalk in Burn Injury.International journal of molecular sciences · 2025
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70 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

4 authors at 1 institution in 1 country.

Yuk Cheung ChanDepartment of Surgery, Davis Heart and Lung Research Institute, The Ohio State University Medical Center, Columbus, Ohio 43210, USA.
Savita Khanna
Sashwati Roy
Chandan K Sen
The Ohio State University Wexner Medical Center · US

Funding

Redox Control of Wound HealingR01GM069589 · NIGMS · OHIO STATE UNIVERSITY · PI SEN, CHANDAN K · 2004 to 2013
$2.3M
Tissue Oxygenation and Wound HealingR01GM077185 · NIGMS · OHIO STATE UNIVERSITY · PI SEN, CHANDAN K · 2007 to 2016
$2.3M
Mechanisms underlying impaired diabetic wound healingR01DK076566 · NIDDK · OHIO STATE UNIVERSITY · PI ROY, SASHWATI · 2008 to 2011
$1.2M
NIDDK NIH HHS R01 DK076566NIGMS NIH HHS GM069589NIGMS NIH HHS GM077185NIGMS NIH HHS R01 GM069589NIGMS NIH HHS R01 GM077185
6 · The paper itself

Abstract

The miR-200 family plays a crucial role in epithelial to mesenchymal transition via controlling cell migration and polarity. We hypothesized that miR-200b, one miR-200 family member, could regulate angiogenic responses via modulating endothelial cell migration. Delivery of the miR-200b mimic in human microvascular endothelial cells (HMECs) suppressed the angiogenic response, whereas miR-200b-depleted HMECs exhibited elevated angiogenesis in vitro, as evidenced by Matrigel® tube formation and cell migration. Using in silico studies, miR target reporter assay, and Western blot analysis revealed that v-ets erythroblastosis virus E26 oncogene homolog 1 (Ets-1), a crucial angiogenesis-related transcription factor, serves as a novel direct target of miR-200b. Knocking down endogenous Ets-1 simulated an anti-angiogenic response of the miR-200b mimic-transfected cells. Certain Ets-1-associated genes, namely matrix metalloproteinase 1 and vascular endothelial growth factor receptor 2, were negatively regulated by miR-200b. Overexpression of Ets-1 rescued miR-200b-dependent impairment in angiogenic response and suppression of Ets-1-associated gene expression. Both hypoxia as well as HIF-1α stabilization inhibited miR-200b expression and elevated Ets-1 expression. Experiments to identify how miR-200b modulates angiogenesis under a low oxygen environment illustrated that hypoxia-induced miR-200b down-regulation de-repressed Ets-1 expression to promote angiogenesis. This study provides the first evidence that hypoxia-sensitive miR-200b is involved in induction of angiogenesis via directly targeting Ets-1 in HMECs.

Indexed as

Cell HypoxiaCell MovementCells, CulturedDown-RegulationEndothelial CellsGene Knockdown TechniquesHumansMicroRNAsNeovascularization, PhysiologicProto-Oncogene Protein c-ets-1Retroviridae Proteins, OncogenicETS1 protein, humanMicroRNAsMIRN200 microRNA, humanoncogene proteins v-etsProto-Oncogene Protein c-ets-1Retroviridae Proteins, Oncogenic

Identifiers

PMID21081489
PMCPMC3023502
OpenAlexW1965176643

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.