Evidence map›Paper›PMID 32572506›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2020

MESP2 variants contribute to conotruncal heart defects by inhibiting cardiac neural crest cell proliferation.

Erge Zhang, Jianping Yang, Yang Liu, Nanchao Hong, Huilin Xie, Qihua Fu, Fen Li, Sun Chen, Yu Yu, Kun Sun

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 46% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
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

10 authors at 2 institutions in 1 country.

Erge ZhangDepartment of Pediatric Cardiovascular, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, 1665 Kongjiang Road, Shanghai, 200092, China.
Jianping YangDepartment of Pediatric Cardiovascular, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, 1665 Kongjiang Road, Shanghai, 200092, China.
Yang LiuDepartment of Pediatric Cardiovascular, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, 1665 Kongjiang Road, Shanghai, 200092, China.
Nanchao HongDepartment of Pediatric Cardiovascular, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, 1665 Kongjiang Road, Shanghai, 200092, China.
Huilin XieDepartment of Pediatric Cardiovascular, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, 1665 Kongjiang Road, Shanghai, 200092, China.
Qihua FuMedical Laboratory, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Fen LiDepartment of Pediatric Cardiology, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Sun ChenDepartment of Pediatric Cardiovascular, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, 1665 Kongjiang Road, Shanghai, 200092, China.
Yu YuDepartment of Pediatric Cardiovascular, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, 1665 Kongjiang Road, Shanghai, 200092, China. yuyu@xinhuamed.com.cn.ORCID http://orcid.org/0000-0001-7783-4618
Kun SunDepartment of Pediatric Cardiovascular, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, 1665 Kongjiang Road, Shanghai, 200092, China. sunkun@xinhuamed.com.cn.
XinHua Hospital · CNShanghai Children's Medical Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Conotruncal heart defects (CTDs) are closely related to defective outflow tract (OFT) development, in which cardiac neural crest cells (CNCCs) play an indispensable role. However, the genetic etiology of CTDs remains unclear. Mesoderm posterior 2 (MESP2) is an important transcription factor regulating early cardiogenesis. Nevertheless, MESP2 variants have not been reported in congenital heart defect (CHD) patients. We first identified four MESP2 variants in 601 sporadic nonsyndromic CTD patients that were not detected in 400 healthy controls using targeted sequencing. Reverse transcription-quantitative PCR (RT-qPCR), immunohistochemistry, and immunofluorescence assays revealed MESP2 expression in the OFT of Carnegie stage (CS) 11, CS13, and CS15 human embryos and embryonic day (E) 8.5, E10, and E11.5 mouse embryos. Functional analyses in HEK 293T cells, HL-1 cells, JoMa1 cells, and primary mouse CNCCs revealed that MESP2 directly regulates the transcriptional activities of downstream CTD-related genes and promotes CNCC proliferation by regulating cell cycle factors. Three MESP2 variants, c.346G>C (p.G116R), c.921C>G (p.Y307X), and c.59A>T (p.Q20L), altered the transcriptional activities of MYOCD, GATA4, NKX2.5, and CFC1 and inhibited CNCC proliferation by upregulating p21

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCell CycleCell LineCell ProliferationDown-RegulationEmbryo, MammalianGene Expression RegulationGenetic VariationHeartHeart Defects, CongenitalHEK293 CellsHumansMiceMyocardiumNeural CrestBasic Helix-Loop-Helix ProteinsMESP2 protein, humanTranscription FactorsCardiac neural crest cellCell cycle factorConotruncal heart defectMESP2Outflow tract

Identifiers

PMID32572506
OpenAlexW3036103770

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.