Evidence map›Paper›PMID 31493044›Full record

ArticleCellular and molecular neurobiology2020

Bcl-2 Overexpression Induces Neurite Outgrowth via the Bmp4/Tbx3/NeuroD1 Cascade in H19-7 Cells.

Yun Young Lee, Hye-Jin Choi, So Young Lee, Shin-Young Park, Min-Jeong Kang, Jinil Han, Joong-Soo Han

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

9 citing papers in PubMed, 9 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

7 authors at 2 institutions in 1 country.

Yun Young LeeDepartment of Biomedical Sciences, Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, 04763, Republic of Korea.
Hye-Jin ChoiBiomedical Research Institute and Department of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, 04763, Republic of Korea.
So Young LeeDepartment of Biomedical Sciences, Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, 04763, Republic of Korea.
Shin-Young ParkBiomedical Research Institute and Department of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, 04763, Republic of Korea.
Min-Jeong KangDepartment of Biomedical Sciences, Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, 04763, Republic of Korea.
Jinil HanDepartment of Biomedical Sciences, Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, 04763, Republic of Korea.
Joong-Soo HanDepartment of Biomedical Sciences, Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, 04763, Republic of Korea. jshan@hanyang.ac.kr.ORCID http://orcid.org/0000-0002-0875-6158
Hanyang University · KRDongwha Pharm (South Korea) · KR

Funding

Hayang University HY-2019Ministry of Health & Welfare, Republic of Korea HI19C0611National Research Foundation of Korea NRF-2013R1A1A2061420National Research Foundation of Korea NRF-2016R1A2B4015358
6 · The paper itself

Abstract

Bcl-2 is overexpressed in the nervous system during neural development and plays an important role in modulating cell survival. In addition to its anti-apoptotic function, it has been suggested previously that Bcl-2 might act as a mediator of neuronal differentiation. However, the mechanism by which Bcl-2 might influence neurogenesis is not sufficiently understood. In this study, we aimed to determine the non-apoptotic functions of Bcl-2 during neuronal differentiation. First, we used microarrays to analyze the whole-genome expression patterns of rat neural stem cells overexpressing Bcl-2 and found that Bcl-2 overexpression induced the expression of various neurogenic genes. Moreover, Bcl-2 overexpression increased the neurite length as well as expression of Bmp4, Tbx3, and proneural basic helix-loop-helix genes, such as NeuroD1, NeuroD2, and Mash1, in H19-7 rat hippocampal precursor cells. To determine the hierarchy of these molecules, we selectively depleted Bmp4, Tbx3, and NeuroD1 in Bcl-2-overexpressing cells. Bmp4 depletion suppressed the upregulation of Tbx3 and NeuroD1 as well as neurite outgrowth, which was induced by Bcl-2 overexpression. Although Tbx3 knockdown repressed Bcl-2-mediated neurite elaboration and downregulated NeuroD1 expression, it did not affect Bcl-2-induced Bmp4 expression. While the depletion of NeuroD1 had no effect on the expression of Bcl-2, Bmp4, or Tbx3, Bcl-2-mediated neurite outgrowth was suppressed. Taken together, these results demonstrate that Bcl-2 regulates neurite outgrowth through the Bmp4/Tbx3/NeuroD1 cascade in H19-7 cells, indicating that Bcl-2 may have a direct role in neuronal development in addition to its well-known anti-apoptotic function in response to environmental insults.

Indexed as

Neuronal OutgrowthAnimalsBasic Helix-Loop-Helix ProteinsBone Morphogenetic Protein 4Cell DifferentiationGene Expression RegulationHippocampusNeural Stem CellsNeuritesNeuropeptidesProto-Oncogene Proteins c-bcl-2Rats, Sprague-DawleySignal TransductionSmad ProteinsT-Box Domain ProteinsBasic Helix-Loop-Helix ProteinsBone Morphogenetic Protein 4Neurod1 protein, ratNeurod2 protein, ratNeuropeptidesProto-Oncogene Proteins c-bcl-2Smad ProteinsT-Box Domain ProteinsTbx3 protein, ratBcl-2Bmp4Neurite outgrowthNeuroD1Tbx3

Identifiers

PMID31493044
PMCPMC11448937
OpenAlexW2971781545

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.