Abnormal gene expression in regular and aggregated somatic cell nuclear transfer placentas.

Bo-Woong Sim, Chae-Won Park, Myung-Hwa Kang, Kwan-Sik Min

Open access · goldAbstract read

In one paragraph

Article in BMC biotechnology, 2017. 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

3.2field-weighted citation impact, top 8% 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

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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, 16 citations in OpenAlex.

Roles of N-linked and O-linked glycosylation sites in the activity of equine chorionic gonadotropin in cells expressing rat luteinizing hormone/chorionic gonadotropin receptor and follicle-stimulating hormone receptor.BMC biotechnology · 2021
Article
Luteinizing hormone-like and follicle-stimulating hormone-like activities of equine chorionic gonadotropin β-subunit mutants in cells expressing rat luteinizing hormone/chorionic gonadotropin receptor and rat follicle-stimulating hormone receptor.Animal cells and systems · 2021
Article
Comparative gene expression profiling of mouse ovaries upon stimulation with natural equine chorionic gonadotropin (N-eCG) and tethered recombinant-eCG (R-eCG).BMC biotechnology · 2020
Article
Transcriptome-wide analysis of the SCNT bovine abnormal placenta during mid- to late gestation.Scientific reports · 2019
Article
Transcriptional defects and reprogramming barriers in somatic cell nuclear reprogramming as revealed by single-embryo RNA sequencing.BMC genomics · 2018
Article

4 · The record

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5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Bo-Woong SimAnimal Biotechnology, Graduate School of Future Convergence Technology, Institute of Genetic Engineering, Hankyong National University, Ansung, 17579, Korea.

Chae-Won ParkAnimal Biotechnology, Graduate School of Future Convergence Technology, Institute of Genetic Engineering, Hankyong National University, Ansung, 17579, Korea.

Myung-Hwa KangDepartment of Food and Nutrition, Hoseo University, Asan, 31499, Korea.

Kwan-Sik MinAnimal Biotechnology, Graduate School of Future Convergence Technology, Institute of Genetic Engineering, Hankyong National University, Ansung, 17579, Korea. ksmin@hknu.ac.kr.

Hankyong National University · KRHoseo University · KRKorea Research Institute of Bioscience and Biotechnology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPlacental defects in somatic cell nuclear transfer (SCNT) are a major cause of complications during pregnancy. One of the most critical factors for the success of SCNT is the successful epigenetic reprogramming of donor cells. Recently, it was reported that the placental weight in mice cloned with the aggregated SCNT method was significantly reduced. Here, we examine the profile of abnormal gene expression using microarray technology in both regular SCNT and aggregated SCNT placentas as well as in vivo fertilization placentas. One SCNT embryo was aggregated with two 2 to 4 -cell stage tetraploid embryos from B6D2F1 mice (C57BL/6 × DBA/2).

resultsIn SCNT placentas, 206 (1.6%) of the 12,816 genes probed were either up-regulated or down-regulated by more than two-fold. However, 52 genes (0.4%) showed differential expression in aggregated SCNT placentas compared to that in controls. In comparison of both types of SCNT placentas with the controls, 33 (92%) out of 36 genes were found to be up-regulated (>2-fold) in SCNT placentas. Among 36 genes, 13 (36%) genes were up-regulated in the aggregated SCNT placentas. Eighty-five genes were down-regulated in SCNT placentas compared with the controls. However, only 9 (about 10.5%) genes were down-regulated in the aggregated SCNT placentas. Of the 34 genes known as imprinted genes, expression was lower in SCNT placentas than that in the controls. Thus, these genes may be the cause of placentomegaly in mice produced post SCNT.

conclusionsThese results suggest that placentomegaly in the SCNT placentas was probably caused by abnormal expression of multiple genes. Taken together, these results suggest that abnormal gene expression in cloned placentas was reduced in a genome-wide manner using the aggregation method with tetraploid embryos.

Indexed as

Nuclear Transfer TechniquesAnimalsCells, CulturedFemaleGene Expression ProfilingGene Expression RegulationHybrid CellsMiceOocytesPlacentaPregnancyProteomeProteomeAbnormal gene expressionAggregated SCNTPlacenta

Identifiers

PMID28347305

DOI10.1186/s12896-017-0355-4

PMCPMC5368936

OpenAlexW2598687801

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LicenceCC BY

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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.