Evidence map›Paper›PMID 34624439›Full record

ArticleMolecular and cellular endocrinology2022

Cellular junction and mesenchymal factors delineate an endometriosis-specific response of endometrial stromal cells to the mesothelium.

Li-Ling Lin, Simran Makwana, Meizhen Chen, Chiou-Miin Wang, Laurel H Gillette, Tim H Huang, Richard O Burney, Bruce J Nicholson, Nameer B Kirma

Open access · hybridAbstract read
In one paragraph

Article in Molecular and cellular endocrinology, 2022. 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
0.8field-weighted citation impact, top 26% 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, 7 citations in OpenAlex.

  1. Review
  2. Review
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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

9 authors at 2 institutions in 1 country.

Li-Ling LinDepartment of Molecular Medicine, University of Texas Health San Antonio, San Antonio, TX, USA.
Simran MakwanaDepartment of Molecular Medicine, University of Texas Health San Antonio, San Antonio, TX, USA.
Meizhen ChenDepartment of Molecular Medicine, University of Texas Health San Antonio, San Antonio, TX, USA.
Chiou-Miin WangDepartment of Molecular Medicine, University of Texas Health San Antonio, San Antonio, TX, USA.
Laurel H GilletteMadigan Army Medical Center, Tacoma, WA, USA.
Tim H HuangDepartment of Molecular Medicine, University of Texas Health San Antonio, San Antonio, TX, USA.
Richard O BurneyMadigan Army Medical Center, Tacoma, WA, USA.
Bruce J NicholsonDepartment of Biochemistry and Structural Biology, University of Texas Health San Antonio, Texas, USA. Electronic address: nicholsonb@uthscsa.edu.
Nameer B KirmaDepartment of Molecular Medicine, University of Texas Health San Antonio, San Antonio, TX, USA. Electronic address: kirma@uthscsa.edu.
The University of Texas Health Science Center at San Antonio · USMadigan Army Medical Center · US

Funding

Molecular mechanisms of gap junction promotion of lesion formation in EndometriosisR01HD109027 · NICHD · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI NICHOLSON, BRUCE J · 2021 to 2025
$2.3M
NICHD NIH HHS R01 HD109027
6 · The paper itself

Abstract

Endometriosis is a debilitating gynecologic disorder that affects ∼10% of women of reproductive age. Endometriosis is characterized by growth of endometriosis lesions within the abdominal cavity, generally thought to arise from retrograde menstruation of shed endometrial tissue. While the pathophysiology underlying peritoneal endometriosis lesion formation is still unclear, the interaction between invading endometrial tissue and the peritoneal mesothelial lining is an essential step in lesion formation. In this study, we assessed proteomic differences between eutopic endometrial stromal cells (ESCs) from women with and without endometriosis in response to peritoneal mesothelial cell (PMC) exposure, using single-cell cytometry by time-of-flight (CyTOF). Co-cultured primary eutopic ESCs from women with and without endometriosis with an established PMC line were subjected to immunostaining with a panel of Maxpar CyTOF metal-conjugated antibodies (n = 28) targeting cell junction and mesenchymal markers, which are involved in cell-cell adhesions and epithelial-mesenchymal transition. Exposure of the ESCs to PMCs resulted in a drastic shift in cellular expression profiles in ESCs derived from endometriosis, whereas little effect by PMCs was observed in ESCs from non-endometriosis subjects. The transcription factor SNAI1 was consistently repressed by PMC interactions. ESCs from endometriosis patients are unique in that they respond to PMCs by undergoing changes in adhesive properties and mesenchymal characteristics that would facilitate lesion formation.

Indexed as

BiomarkersCells, CulturedCoculture TechniquesComputational BiologyEndometriosisEndometriumEpithelial CellsEpitheliumFemaleHumansIntercellular JunctionsProteomicsSingle-Cell AnalysisStromal CellsBiomarkersCellular adhesionCyTOFEndometriosisMass cytometryMesenchymal factors

Identifiers

PMID34624439
PMCPMC12048087
OpenAlexW3204674933

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.