Evidence map›Paper›PMID 33862275›Full record

ArticleCellular and molecular gastroenterology and hepatology2021

Longitudinal Single-Cell Transcriptomics Reveals a Role for Serpina3n-Mediated Resolution of Inflammation in a Mouse Colitis Model.

Yen-Ting Ho, Takashi Shimbo, Edward Wijaya, Tomomi Kitayama, Satoshi Takaki, Kentaro Ikegami, Kazuya Miyashita, Yuya Ouchi, Eiichi Takaki, Ryoma Yamamoto and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
6.8field-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.

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

35 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Nat10-mediated acScience China. Life sciences · 2026
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  6. Longitudinal omics data analysis: approaches and applications.Computational and structural biotechnology journal · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Yen-Ting HoDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Japan.
Takashi ShimboDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Japan. Electronic address: shimbot@sts.med.osaka-u.ac.jp.
Edward WijayaDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Japan; StemRIM Inc, Ibaraki, Osaka, Japan.
Tomomi KitayamaDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Japan; StemRIM Inc, Ibaraki, Osaka, Japan.
Satoshi TakakiDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Japan.
Kentaro IkegamiStemRIM Inc, Ibaraki, Osaka, Japan.
Kazuya MiyashitaStemRIM Inc, Ibaraki, Osaka, Japan.
Yuya OuchiDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Japan; StemRIM Inc, Ibaraki, Osaka, Japan.
Eiichi TakakiDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Japan; StemRIM Inc, Ibaraki, Osaka, Japan.
Ryoma YamamotoDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Japan; StemRIM Inc, Ibaraki, Osaka, Japan.
Yasufumi KanedaDivision of Gene Therapy Science, Graduate School of Medicine, Osaka University, Suita, Japan.
Katsuto TamaiDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Japan.
The University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsProper resolution of inflammation is essential to maintaining homeostasis, which is important as a dysregulated inflammatory response has adverse consequences, even being regarded as a hallmark of cancer. However, our picture of dynamic changes during inflammation remains far from comprehensive.

methodsHere we used single-cell transcriptomics to elucidate changes in distinct cell types and their interactions in a mouse model of chemically induced colitis.

resultsOur analysis highlights the stromal cell population of the colon functions as a hub with dynamically changing roles over time. Importantly, we found that Serpina3n, a serine protease inhibitor, is specifically expressed in stromal cell clusters as inflammation resolves, interacting with a potential target, elastase. Indeed, genetic ablation of the Serpina3n gene delays resolution of induced inflammation. Furthermore, systemic Serpina3n administration promoted the resolution of inflammation, ameliorating colitis symptoms.

conclusionsThis study provides a comprehensive, single-cell understanding of cell-cell interactions during colorectal inflammation and reveals a potential therapeutic target that leverages inflammation resolution.

Indexed as

Single-Cell AnalysisAcute-Phase ProteinsAnimalsCell CommunicationColitisColonDextran SulfateDisease Models, AnimalGenetic Predisposition to DiseaseInflammationInflammatory Bowel DiseasesMiceMice, Inbred C57BLPhenotypeRisk FactorsRNA-SeqAcute-Phase ProteinsDextran SulfateSerpina3n protein, mouseSerpinsColitisSerpina3nSingle Cell RNA-SequencingStromal Cell

Identifiers

PMID33862275
PMCPMC8258998
OpenAlexW3156774813

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.