Evidence map›Paper›PMID 29688269›Full record

ArticleBiology of reproduction2018

Polycystic ovary syndrome: possible involvement of androgen-induced, chemerin-mediated ovarian recruitment of monocytes/macrophages.

Patricia D A Lima, Anne-Laure Nivet, Qi Wang, Yi-An Chen, Arthur Leader, Annie Cheung, Chii-Ruey Tzeng, Benjamin K Tsang

Open access · bronzeAbstract read
In one paragraph

Article in Biology of reproduction, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 2 pooled it
9.2field-weighted citation impact, top 2% 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

71 citing papers in PubMed, 2 syntheses or guidelines pooled it, 122 citations in OpenAlex.

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11 more citing papers are in PubMed but not listed here.

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

8 authors at 5 institutions in 5 countries.

Patricia D A LimaDepartments of Obstetrics & Gynecology and Cellular & Molecular Medicine, Interdisciplinary School of Health Sciences, University of Ottawa; Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
Anne-Laure NivetDepartments of Obstetrics & Gynecology and Cellular & Molecular Medicine, Interdisciplinary School of Health Sciences, University of Ottawa; Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
Qi WangDepartments of Obstetrics & Gynecology and Cellular & Molecular Medicine, Interdisciplinary School of Health Sciences, University of Ottawa; Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
Yi-An ChenCenter for Reproductive Medicine and Science, Taipei Medical University Hospital, Taipei, Taiwan.
Arthur LeaderThe Ottawa Fertility Centre, Ottawa, Ontario, Canada.
Annie CheungDepartment of Pathology, University of Hong Kong, University Pathology Building, Queen Mary Hospital, Pokfulam Road, Hong Kong, People's Republic of China.
Chii-Ruey TzengCenter for Reproductive Medicine and Science, Taipei Medical University Hospital, Taipei, Taiwan.
Benjamin K TsangDepartments of Obstetrics & Gynecology and Cellular & Molecular Medicine, Interdisciplinary School of Health Sciences, University of Ottawa; Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
University of Ottawa · CATaipei Medical University Hospital · TWMacau University of Science and Technology · MOOttawa Fertility Centre · CAQueen Mary Hospital · CN

Funding

CIHR MOP-119381
6 · The paper itself

Abstract

Polycystic ovary syndrome (PCOS) is a continuum of endocrine and reproductive disorders characterized by hyperandrogenism, antral follicle growth arrest, and chronic inflammation. Macrophages play key role in inflammation, and the balance between M1 (inflammatory) and M2 (anti-inflammatory) macrophages determines physiological/pathological outcomes. Here, we investigated if hyperandrogenism increases ovarian chemerin altering the balance of M1 and M2 macrophages and the granulosa cell death. Ovarian chemerin was upregulated by 5α-dihydrotestosterone (DHT) in lean and overweight rats; while increased serum chemerin levels were only evident in overweight rats, suggesting that the serum chemerin may be reflective of a systemic response and associated with obesity, whereas increased ovarian chemerin expression is a localized response independent of the metabolic status. DHT altered follicle dynamics while increased the M1: M2 macrophages ratio in antral and pre-ovulatory follicles. While ovarian M1 macrophages expressing chemokine-like receptor 1 (CMKLR1) were increased, CMKLR1+ monocytes, which migrated toward chemerin-rich environment, were markedly decreased after 15 days of DHT. Androgen-induced granulosa cell apoptosis was dependent on the presence of macrophages. In humans, chemerin levels in follicular fluid, but not in serum, were higher in lean PCOS patients compared to BMI-matched controls and were associated with increased M1: M2 ratio. Our results support the concept that in PCOS, hyperandrogenemia increases chemerin expression while promotes CMKLR1+ monocytes recruitment and deregulates the immunological niche of ovaries. This study established a new immunological perspective in PCOS at the ovarian level. Hyperandrogenism is associated with upregulation of chemerin and macrophage unbalance in the ovaries.

Indexed as

AndrogensAnimalsApoptosisCell MovementChemokinesDihydrotestosteroneDisease Models, AnimalFemaleGranulosa CellsHumansHyperandrogenismIntercellular Signaling Peptides and ProteinsMacrophagesMonocytesOvaryPolycystic Ovary SyndromeAndrogensChemokinesCmklr1 protein, ratDihydrotestosteroneIntercellular Signaling Peptides and ProteinsRARRES2 protein, humanRarres2 protein, ratReceptors, Chemokine

Identifiers

PMID29688269
PMCPMC6203875
OpenAlexW2802321345

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.