Evidence map›Paper›PMID 38498294›Full record

ArticleStem cell reviews and reports2024

Development of an Inflamed High Throughput Stem-cell-based Gut Epithelium Model to Assess the Impact of Annexin A1.

Milena Fronza Broering, Stefania Tocci, Noah T Sout, Chris Reutelingsperger, Sandra H P Farsky, Soumita Das, Ibrahim M Sayed

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Article in Stem cell reviews and reports, 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
1.2field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 5 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

7 authors at 3 institutions in 3 countries.

Milena Fronza BroeringDepartment of Biomedical and Nutritional Sciences, University of Massachusetts-Lowell, Lowell, MA, 01854, USA.
Stefania TocciDepartment of Biomedical and Nutritional Sciences, University of Massachusetts-Lowell, Lowell, MA, 01854, USA.
Noah T SoutDepartment of Biomedical and Nutritional Sciences, University of Massachusetts-Lowell, Lowell, MA, 01854, USA.
Chris ReutelingspergerCardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht University, Maastricht, 6211 LK, The Netherlands.
Sandra H P FarskyDepartment of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of Sao Paulo, São Paulo, São Paulo, 05508-000, Brazil.
Soumita DasDepartment of Biomedical and Nutritional Sciences, University of Massachusetts-Lowell, Lowell, MA, 01854, USA. soumita_das@uml.edu.
Ibrahim M SayedDepartment of Biomedical and Nutritional Sciences, University of Massachusetts-Lowell, Lowell, MA, 01854, USA. ibrahim_ibrahim@uml.edu.ORCID 0000-0001-8207-6401
University of Massachusetts Lowell · USMaastricht University · NLUniversidade de São Paulo · BR

Funding

Innate responses following infection with enteric microbesR01DK107585 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DAS, SOUMITA · 2016 to 2020
$2.2M
Conselho Nacional de Desenvolvimento Científico e Tecnológico Conselho Nacional de Desenvolvimento Científico e TecnológicoFundação de Amparo à Pesquisa do Estado de São Paulo Fundação de Amparo à Pesquisa do Estado de São PauloLeona M. and Harry B. Helmsley Charitable Trust Leona M. and Harry B. Helmsley Charitable TrustNIDDK NIH HHS R01 DK107585
6 · The paper itself

Abstract

OBJECTIVE AND

designAnnexin A1 (ANXA1) plays a role in maintaining intestinal hemostasis, especially following mucosal inflammation. The published data about ANXA1 was derived from experimental animal models where there is an overlapping between epithelial and immune cells. There is no in vitro gut epithelial model that can assess the direct effect of ANXA1 on the gut epithelium.

methodsWe developed high-throughput stem-cell-based murine epithelial cells and bacterial lipopolysaccharides (LPS) were used to induce inflammation. The impact of ANXA1 and its functional part (Ac2-26) was evaluated in the inflamed model. Intestinal integrity was assessed by the transepithelial electrical resistance (TEER), and FITC-Dextran permeability. Epithelial junction proteins were assessed using confocal microscopy and RT-qPCR. Inflammatory cytokines were evaluated by RT-qPCR and ELISA.

resultsLPS challenge mediated a damage in the epithelial cells as shown by a drop in the TEER and an increase in FITC-dextran permeability; reduced the expression of epithelial junctional proteins (Occludin, ZO-1, and Cadherin) and increased the expression of the gut leaky protein, Claudin - 2. ANXA1 and Ac2-26 treatment reduced the previous damaging effects. In addition, ANXA1 and Ac2-26 inhibited the inflammatory responses mediated by the LPS and increased the transcription of the anti-inflammatory cytokine, IL-10.

conclusionANXA1 and Ac2-26 directly protect the epithelial integrity by affecting the expression of epithelial junction and inflammatory markers. The inflamed gut model is a reliable tool to study intestinal inflammatory diseases, and to evaluate the efficacy of potential anti-inflammatory drugs and the screening of new drugs that could be candidates for inflammatory bowel disease.

Indexed as

Annexin A1InflammationIntestinal MucosaLipopolysaccharidesAnimalsCytokinesEpithelial CellsMicePeptidesPermeabilityStem CellsAnnexin A1annexin A1 peptide (2-26)CytokinesLipopolysaccharidesPeptides3D OrganoidsAnnexin1High-throughput (HTP) cell ModelInflamed ModelPolarized Epithelial Cells

Identifiers

PMID38498294
OpenAlexW4392926522

What OpenQuestion holds

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Registered trials

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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.