Evidence map›Paper›PMID 31901086›Full record

ArticleBiology of reproduction2020

The autophagy protein, FIP200 (RB1CC1) mediates progesterone responses governing uterine receptivity and decidualization†.

Arin K Oestreich, Sangappa B Chadchan, Alexandra Medvedeva, John P Lydon, Emily S Jungheim, Kelle H Moley, Ramakrishna Kommagani

Open access · greenAbstract read
In one paragraph

Article in Biology of reproduction, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

27 citing papers in PubMed, 44 citations in OpenAlex.

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  20. The Multifaceted Role of Autophagy in Endometrium Homeostasis and Disease.Reproductive sciences (Thousand Oaks, Calif.) · 2022
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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 2 institutions in 1 country.

Arin K OestreichDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, MO, 63110, USA and.
Sangappa B ChadchanDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, MO, 63110, USA and.
Alexandra MedvedevaDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, MO, 63110, USA and.
John P LydonDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, 77030, USA.
Emily S JungheimDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, MO, 63110, USA and.
Kelle H MoleyDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, MO, 63110, USA and.
Ramakrishna KommaganiDepartment Obstetrics and Gynecology, Center for Reproductive Health Sciences, Washington University School of Medicine, St. Louis, MO, 63110, USA and.
Washington University in St. Louis · USBaylor College of Medicine · US

Funding

DIABETES &RELATED METABOLIC DISEASEST32DK007120 · NIDDK · WASHINGTON UNIVERSITY · PI MARCO COLONNA, Maria Sara Remedi · 1986 to 2026
$15.7M
Molecular Analysis of Uterine ReceptivityR01HD042311 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI LYDON, JOHN P · 2009 to 2023
$4.8M
MOLECULAR AND METABOLIC ASPECTS OF IMPLANTATIONR01HD065435 · NICHD · WASHINGTON UNIVERSITY · PI KOMMAGANI, RAMAKRISHNA, SANTI, CELIA M · 2010 to 2020
$4.5M
SLO3 KO MOUSE: A TOOL TO REVEAL VOLTAGE-DEPENDENT PROCESSES IN SPERM FERTILITYR01HD069631 · NICHD · WASHINGTON UNIVERSITY · PI SANTI, CELIA M · 2011 to 2022
$3.3M
Maternal nutrition and oocyte programmingR01HD083895 · NICHD · WASHINGTON UNIVERSITY · PI ENGLAND, SARAH K. · 2015 to 2019
$2.7M
GREB1 Action in Endometrial Function and DysfunctionR00HD080742 · NICHD · WASHINGTON UNIVERSITY · PI KOMMAGANI, RAMAKRISHNA · 2017 to 2019
$702k
NICHD NIH HHS R00 HD080742NICHD NIH HHS R01 HD042311NICHD NIH HHS R01 HD065435NICHD NIH HHS R01 HD069631NICHD NIH HHS R01 HD083895NIDDK NIH HHS T32 DK007120
6 · The paper itself

Abstract

Successful establishment of pregnancy depends on steroid hormone-driven cellular changes in the uterus during the peri-implantation period. To become receptive to embryo implantation, uterine endometrial stromal cells (ESCs) must transdifferentiate into decidual cells that secrete factors necessary for embryo survival and trophoblast invasion. Autophagy is a key homeostatic process vital for cellular homeostasis. Although the uterus undergoes major cellular changes during early pregnancy, the precise role of autophagy in uterine function is unknown. Here, we report that conditional knockout of the autophagy protein FIP200 in the reproductive tract of female mice results in reduced fecundity due to an implantation defect. In the absence of FIP200, aberrant progesterone signaling results in sustained uterine epithelial proliferation and failure of stromal cells to decidualize. Additionally, loss of FIP200 impairs decidualization of human ESCs. We conclude that the autophagy protein FIP200 plays a crucial role in uterine receptivity, decidualization, and fertility. These data establish autophagy as a major cellular pathway required for uterine receptivity and decidualization in both mice and human ESCs.

Indexed as

AnimalsAutophagyAutophagy-Related ProteinsDeciduaEmbryo ImplantationEndometriumFemaleHumansMiceMice, KnockoutProgesteroneSignal TransductionStromal CellsUterusAutophagy-Related ProteinsProgesteroneRb1cc1 protein, mouseendometriumfertilityhESCsimplantationPR-Crepregnancy

Identifiers

PMID31901086
PMCPMC7124967
OpenAlexW2997641852

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.