Evidence map›Paper›PMID 25468940›Full record

ArticleDevelopment (Cambridge, England)2014

Sirh7/Ldoc1 knockout mice exhibit placental P4 overproduction and delayed parturition.

Mie Naruse, Ryuichi Ono, Masahito Irie, Kenji Nakamura, Tamio Furuse, Toshiaki Hino, Kanako Oda, Misho Kashimura, Ikuko Yamada, Shigeharu Wakana and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

41 citing papers in PubMed, 73 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

13 authors at 5 institutions in 1 country.

Mie NaruseDepartment of Epigenetics, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan School of Health Sciences, Tokai University, Bohseidai, Isehara, Kanagawa 259-1193, Japan.
Ryuichi OnoDepartment of Epigenetics, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan.
Masahito IrieDepartment of Epigenetics, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan School of Health Sciences, Tokai University, Bohseidai, Isehara, Kanagawa 259-1193, Japan.
Kenji NakamuraMitsubishi Kagaku Institute of Life Sciences, 11 Minamiooya, Machida, Tokyo 194-8511, Japan Faculty of Medicine, Tokai University, Bohseidai, Isehara, Kanagawa 259-1193, Japan.
Tamio FuruseTechnology and Development Team for Mouse Phenotype Analysis, The Japan Mouse Clinic, RIKEN BRC, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan.
Toshiaki HinoMitsubishi Kagaku Institute of Life Sciences, 11 Minamiooya, Machida, Tokyo 194-8511, Japan Department of Biological Sciences, Asahikawa Medical University, 2-1-1-1 Midorigaoka-higashi, Asahikawa 078-8510, Japan.
Kanako OdaMitsubishi Kagaku Institute of Life Sciences, 11 Minamiooya, Machida, Tokyo 194-8511, Japan Brain Research Institute, Niigata University, 1-757 Asahimachi-dori, Niigata 951-8585, Japan.
Misho KashimuraTechnology and Development Team for Mouse Phenotype Analysis, The Japan Mouse Clinic, RIKEN BRC, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan.
Ikuko YamadaTechnology and Development Team for Mouse Phenotype Analysis, The Japan Mouse Clinic, RIKEN BRC, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan.
Shigeharu WakanaTechnology and Development Team for Mouse Phenotype Analysis, The Japan Mouse Clinic, RIKEN BRC, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan.
Minesuke YokoyamaMitsubishi Kagaku Institute of Life Sciences, 11 Minamiooya, Machida, Tokyo 194-8511, Japan Brain Research Institute, Niigata University, 1-757 Asahimachi-dori, Niigata 951-8585, Japan.
Fumitoshi IshinoDepartment of Epigenetics, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan Global Center of Excellence Program for International Research Center for Molecular Science in Tooth and Bone Diseases, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan fishino.epgn@mri.tmd.ac.jp tkanekoi@is.icc.u-tokai.ac.jp.
Tomoko Kaneko-IshinoSchool of Health Sciences, Tokai University, Bohseidai, Isehara, Kanagawa 259-1193, Japan fishino.epgn@mri.tmd.ac.jp tkanekoi@is.icc.u-tokai.ac.jp.
RIKEN BioResource Research Center · JPTokyo Medical and Dental University · JPMitsubishi Group (Japan) · JPAsahikawa Medical University · JPTokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sirh7/Ldoc1 [sushi-ichi retrotransposon homolog 7/leucine zipper, downregulated in cancer 1, also called mammalian retrotransposon-derived 7 (Mart7)] is one of the newly acquired genes from LTR retrotransposons in eutherian mammals. Interestingly, Sirh7/Ldoc1 knockout (KO) mice exhibited abnormal placental cell differentiation/maturation, leading to an overproduction of placental progesterone (P4) and placental lactogen 1 (PL1) from trophoblast giant cells (TGCs). The placenta is an organ that is essential for mammalian viviparity and plays a major endocrinological role during pregnancy in addition to providing nutrients and oxygen to the fetus. P4 is an essential hormone in the preparation and maintenance of pregnancy and the determination of the timing of parturition in mammals; however, the biological significance of placental P4 in rodents is not properly recognized. Here, we demonstrate that mouse placentas do produce P4 in mid-gestation, coincident with a temporal reduction in ovarian P4, suggesting that it plays a role in the protection of the conceptuses specifically in this period. Pregnant Sirh7/Ldoc1 knockout females also displayed delayed parturition associated with a low pup weaning rate. All these results suggest that Sirh7/Ldoc1 has undergone positive selection during eutherian evolution as a eutherian-specific acquired gene because it impacts reproductive fitness via the regulation of placental endocrine function.

Indexed as

AnimalsDNA PrimersFemaleGenotypeIn Situ HybridizationMiceMice, KnockoutMifepristoneParturitionPlacentaPlacental LactogenPolymerase Chain ReactionPregnancyProgesteroneReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionDNA PrimersMifepristonePlacental LactogenProgesteroneEvolutionGestationParturitionPlacentaProgesteroneRetrotransposon

Identifiers

PMID25468940
PMCPMC4299276
OpenAlexW1979447516

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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.