Evidence map›Paper›PMID 33428059›Full record

ArticleMolecular and cellular biochemistry2021

Endometriosis stromal cells induce bone marrow mesenchymal stem cell differentiation and PD-1 expression through paracrine signaling.

Peng Chen, Ramanaiah Mamillapalli, Shutaro Habata, Hugh S Taylor

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 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

4 authors at 1 institution in 2 countries.

Peng Chen *Department of Obstetrics, Gynecology and Reproductive Sciences, Yale School of Medicine, 310 Cedar Street, New Haven, CT, 06510, USA.
Ramanaiah Mamillapalli *Department of Obstetrics, Gynecology and Reproductive Sciences, Yale School of Medicine, 310 Cedar Street, New Haven, CT, 06510, USA. ramana.mamillapalli@yale.edu.ORCID http://orcid.org/0000-0002-4022-8910
Shutaro HabataDepartment of Obstetrics, Gynecology and Reproductive Sciences, Yale School of Medicine, 310 Cedar Street, New Haven, CT, 06510, USA.
Hugh S TaylorDepartment of Obstetrics, Gynecology and Reproductive Sciences, Yale School of Medicine, 310 Cedar Street, New Haven, CT, 06510, USA.
Yale University · US

Funding

Boston Center for Endometriosis AWD0003567
6 · The paper itself

Abstract

Endometriosis is an estrogen-dependent, inflammatory gynecological disorder characterized by the growth of endometrial cells in lesions outside the uterus. Bone marrow-derived cells (BMDCs) engraft lesions and increase lesion size. Do endometriosis cells regulate differentiation of engrafted BMDCs in the pathogenesis and growth of endometriosis? Here, we report endometriosis derived stromal cells promote the differentiation of BMDCs to stromal, epithelial and leukocyte cell fates through paracrine signaling. In-vitro studies demonstrated that both mRNA and protein levels of vimentin, cytokeratin and PD-1 were significantly increased in BMDCs cocultured with stromal cells from endometriosis (ENDO) patients compared to stromal cells from normal endometrium (CNTL). Increased expression of PD-1 has been reported in malignancy where it promotes T cell quiescence and immune tolerance. Increased PD-1 was also confirmed in-vivo where we showed that PD-1 expression was induced in BMDCs engrafted into endometriotic lesions in a murine model of endometriosis. AMD3100, an antagonist for CXCR4 receptor inhibited PD-1 expression in BMDCs suggesting that PD-1 induction requires CXCL12. These results suggest that endometriosis stimulated BMDC differentiation through paracrine signaling and increased T cell PD-1 expression. Increased PD-1 expression may be one mechanism by which endometriosis avoids immune surveillance.

Indexed as

Cell DifferentiationGene Expression RegulationParacrine CommunicationAdolescentAdultBone Marrow CellsCoculture TechniquesEndometriosisFemaleHumansMesenchymal Stem CellsMiddle AgedProgrammed Cell Death 1 ReceptorStromal CellsPDCD1 protein, humanProgrammed Cell Death 1 ReceptorBone marrowCK19EndometriosisEndometriumPD-1Vimentin

Identifiers

PMID33428059
OpenAlexW3120130894

What OpenQuestion holds

Textmetadata
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.