Evidence map›Paper›PMID 38329343›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2024

MicroRNA-409-3p/BTG2 signaling axis improves impaired angiogenesis and wound healing in obese mice.

Furkan Bestepe, George F Ghanem, Colette M Fritsche, James Weston, Sumedha Sahay, Amanda K Mauro, Parul Sahu, Sude M Tas, Brooke Ruemmele, Sarah Persing and 5 more

Open access · goldAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

5 citing papers in PubMed, 4 citations in OpenAlex.

  1. Research progress on BTG2 in non‑tumor diseases (Review).International journal of molecular medicine · 2026
    Review
  2. Article
  3. Article
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  5. Review
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

15 authors at 1 institution in 1 country.

Furkan BestepeDepartment of Medicine, Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0000-0002-0451-8224
George F GhanemDepartment of Medicine, Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0009-0005-1229-1946
Colette M FritscheDepartment of Medicine, Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0000-0001-9534-8293
James WestonDepartment of Medicine, Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0000-0001-8269-981X
Sumedha SahayDepartment of Medicine, Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0009-0004-4546-6856
Amanda K MauroDepartment of Medicine, Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0000-0002-4930-2101
Parul SahuDepartment of Medicine, Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0000-0001-8864-4043
Sude M TasDepartment of Medicine, Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0000-0003-3884-1174
Brooke RuemmeleDivision of Plastic and Reconstructive Surgery, Department of Surgery, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0009-0004-1922-7261
Sarah PersingDivision of Plastic and Reconstructive Surgery, Department of Surgery, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0009-0006-6039-1535
Miranda E GoodDepartment of Medicine, Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0000-0001-7775-1863
Abhishek ChatterjeeDivision of Plastic and Reconstructive Surgery, Department of Surgery, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0000-0002-8003-7991
Gordon S HugginsDepartment of Medicine, Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0000-0002-8035-0312
Payam SalehiDivision of Vascular Surgery, Cardiovascular Center, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0000-0001-7482-3753
Basak IcliDepartment of Medicine, Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts, USA.ORCID 0000-0002-4867-8326
Tufts Medical Center · US

Funding

MiR-409-3p Regulates Angiogensis, Brown Fat Adiposity and Insulin ResistanceR01HL149999 · NHLBI · TUFTS MEDICAL CENTER · PI ICLI, BASAK · 2020 to 2024
$3.1M
Vascular Pannexin 1 in Ischemic StrokeR00HL143165 · NHLBI · TUFTS MEDICAL CENTER · PI GOOD, MIRANDA E · 2020 to 2022
$747k
Endothelial Pannexin1 in Alzheimer’s DiseaseR21AG075796 · NIA · TUFTS MEDICAL CENTER · PI GOOD, MIRANDA E · 2022 to 2022
$490k
NHLBI NIH HHS R00 HL143165NHLBI NIH HHS R01 HL149999NIA NIH HHS R21 AG075796
6 · The paper itself

Abstract

Wound healing is facilitated by neoangiogenesis, a complex process that is essential to tissue repair in response to injury. MicroRNAs are small, noncoding RNAs that can regulate the wound healing process including stimulation of impaired angiogenesis that is associated with type-2 diabetes (T2D). Expression of miR-409-3p was significantly increased in the nonhealing skin wounds of patients with T2D compared to the non-wounded normal skin, and in the skin of a murine model with T2D. In response to high glucose, neutralization of miR-409-3p markedly improved EC growth and migration in human umbilical vein endothelial cells (HUVECs), promoted wound closure and angiogenesis as measured by increased CD31 in human skin organoids, while overexpression attenuated EC angiogenic responses. Bulk mRNA-Seq transcriptomic profiling revealed BTG2 as a target of miR-409-3p, where overexpression of miR-409-3p significantly decreased BTG2 mRNA and protein expression. A 3' untranslated region (3'-UTR) luciferase assay of BTG2 revealed decreased luciferase activity with overexpression of miR-409-3p, while inhibition had opposite effects. Mechanistically, in response to high glucose, miR-409-3p deficiency in ECs resulted in increased mTOR phosphorylation, meanwhile BTG-anti-proliferation factor 2 (BTG2) silencing significantly decreased mTOR phosphorylation. Endothelial-specific and tamoxifen-inducible miR-409-3p knockout mice (MiR-409

Indexed as

Diabetes Mellitus, Type 2Immediate-Early ProteinsMicroRNAsTumor Suppressor ProteinsAngiogenesisAnimalsCell ProliferationGlucoseHumansHuman Umbilical Vein Endothelial CellsLuciferasesMiceMice, ObeseRNA, MessengerTOR Serine-Threonine KinasesWound HealingBTG2 protein, humanBtg2 protein, mouseGlucoseImmediate-Early ProteinsLuciferasesMicroRNAsMIRN409 microRNA, humanMIRN409 microRNA, mouseRNA, MessengerTOR Serine-Threonine KinasesTumor Suppressor ProteinsangiogenesisBTG2endothelial cellsmicroRNAsobesitywound healing

Identifiers

PMID38329343
PMCPMC12235660
OpenAlexW4391654421

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.