Evidence map›Paper›PMID 38794128›Full record

ArticlePharmaceuticals (Basel, Switzerland)2024

Unveiling the Role of Tryptophan 2,3-Dioxygenase in the Angiogenic Process.

Marta Cecchi, Cecilia Anceschi, Angela Silvano, Maria Luisa Coniglio, Aurora Chinnici, Lucia Magnelli, Andrea Lapucci, Anna Laurenzana, Astrid Parenti

Abstract read
In one paragraph

Article in Pharmaceuticals (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. 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

9 authors.

Marta CecchiDepartment of Neuroscience, Psychology, Drug Research and Child Health, (NEUROFARBA) Pharmacology and Toxicology Section, University of Florence, 50139 Florence, Italy.ORCID 0000-0002-8777-6674
Cecilia AnceschiDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, 50121 Florence, Italy.
Angela SilvanoDepartment of Health Sciences, Division of Obstetrics and Gynecology, Careggi Hospital, University of Florence, 50134 Florence, Italy.ORCID 0000-0002-7412-823X
Maria Luisa ConiglioCentre of Excellence, Division of Pediatric Oncology/Hematology, Meyer Children's Hospital IRCCS, 50139 Florence, Italy.
Aurora ChinniciDepartment of Neuroscience, Psychology, Drug Research and Child Health, (NEUROFARBA) Pharmacology and Toxicology Section, University of Florence, 50139 Florence, Italy.ORCID 0000-0001-6429-5942
Lucia MagnelliDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, 50121 Florence, Italy.ORCID 0000-0003-4585-1450
Andrea LapucciDepartment of Health Sciences, Clinical Pharmacology and Oncology Section, University of Florence, V. le G. Pieraccini, 6, 50139 Florence, Italy.
Anna LaurenzanaDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, 50121 Florence, Italy.ORCID 0000-0002-8745-3808
Astrid ParentiDepartment of Health Sciences, Clinical Pharmacology and Oncology Section, University of Florence, V. le G. Pieraccini, 6, 50139 Florence, Italy.ORCID 0000-0002-7980-6853

Funding

EU PNRR POCARNO22Regione Toscana Bando Ricerca Salute 2018University of Florence N.A.
6 · The paper itself

Abstract

backgroundIndoleamine 2,3-dioxygenase (IDO1) and tryptophan-2,3-dioxygenase (TDO) are the two principals enzymes involved in the catabolization of tryptophan (Trp) into kynurenine (Kyn). Despite their well-established role in the immune escape, their involvement in angiogenesis remains uncertain. We aimed to characterize TDO and IDO1 in human umbilical venular endothelial cells (HUVECs) and human endothelial colony-forming cells (ECFCs).

methodsqRT-PCR and immunofluorescence were used for TDO and IDO1 expression while their activity was measured using ELISA assays. Cell proliferation was examined via MTT tests and in in vitro angiogenesis by capillary morphogenesis.

resultsHUVECs and ECFCs expressed TDO and IDO1. Treatment with the selective TDO inhibitor 680C91 significantly impaired HUVEC proliferation and 3D-tube formation in response to VEGF-A, while IDO1 inhibition showed no effect. VEGF-induced mTor phosphorylation and Kyn production were hindered by 680C91. ECFC morphogenesis was also inhibited by 680C91. Co-culturing HUVECs with A375 induced TDO up-regulation in both cell types, whose inhibition reduced MMP9 activity and prevented c-Myc and E2f1 upregulation.

conclusionsHUVECs and ECFCs express the key enzymes of the kynurenine pathway. Significantly, TDO emerges as a pivotal player in in vitro proliferation and capillary morphogenesis, suggesting a potential pathophysiological role in angiogenesis beyond its well-known immunomodulatory effects.

Indexed as

angiogenesisendothelial cellsendothelial progenitor cellskynurenine pathwaymelanomametalloproteinasestryptophan 2,3-dioxygenase

Identifiers

PMID38794128
PMCPMC11124529

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.