Evidence map›Paper›PMID 40169106›Full record

ArticleExperimental neurology2025

Neural tube defects induce abnormal astrocyte development by activation and epigenetic permissiveness of STAT3.

Karolina Janik, Li-Qing Jin, Kuralai Zholdosh Kyzy, Rafal Kaminski, George M Smith, Barbara Krynska

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental neurology, 2025. 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
–field-weighted citation impact
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.

  1. Review
  2. Review
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

6 authors.

Karolina JanikDepartment of Neural Sciences, Lewis Katz School of Medicine, Temple University, 3500 North Broad Street, Philadelphia, PA 19140, USA; Center for Neural Development and Repair, Lewis Katz School of Medicine, Temple University, 3500 North Broad Street, Philadelphia, PA 19140, USA.
Li-Qing JinDepartment of Neural Sciences, Lewis Katz School of Medicine, Temple University, 3500 North Broad Street, Philadelphia, PA 19140, USA.
Kuralai Zholdosh KyzyDepartment of Neural Sciences, Lewis Katz School of Medicine, Temple University, 3500 North Broad Street, Philadelphia, PA 19140, USA.
Rafal KaminskiDepartment of Microbiology, Immunology, and Inflammation, Center for NeuroVirology and Gene Editing, Lewis Katz School of Medicine, Temple University, 3500 North Broad Street, Philadelphia, PA 19140, USA.
George M SmithDepartment of Neural Sciences, Lewis Katz School of Medicine, Temple University, 3500 North Broad Street, Philadelphia, PA 19140, USA; Center for Neural Development and Repair, Lewis Katz School of Medicine, Temple University, 3500 North Broad Street, Philadelphia, PA 19140, USA.
Barbara KrynskaDepartment of Neural Sciences, Lewis Katz School of Medicine, Temple University, 3500 North Broad Street, Philadelphia, PA 19140, USA; Center for Neural Development and Repair, Lewis Katz School of Medicine, Temple University, 3500 North Broad Street, Philadelphia, PA 19140, USA. Electronic address: barbara.krynska@temple.edu.

Funding

Viral Gene Editing and Bioinformatics Core for Institution # 269291P30MH092177 · NIMH · TEMPLE UNIV OF THE COMMONWEALTH · PI Ilker Kudret Sariyer · 2011 to 2026
$24.9M
The role of extracellular matrix in MyelomeningoceleR01NS109064 · NINDS · TEMPLE UNIV OF THE COMMONWEALTH · PI KRYNSKA, BARBARA · 2018 to 2022
$1.7M
NIMH NIH HHS P30 MH092177NINDS NIH HHS R01 NS109064
6 · The paper itself

Abstract

The open neural tube defect, myelomeningocele (MMC), is a debilitating congenital defect of the central nervous system, characterized by impaired spinal cord development. The pathological development of MMC spinal cord involves enhanced astrogenesis. However, the mechanisms underlying the abnormal generation of astrocytes in MMC spinal cord are poorly understood. Using a fetal rat model of this defect, we discovered that neural progenitor cells (NPCs) in the developing spinal cord undergo the accelerated acquisition of astrocytic competency and the abnormal induction of GFAP expression, resulting in the enhanced generation of astrocytes. We identified that the activation of signal transducer and activator of transcription 3 (STAT3) in NPCs, accompanied by the early epigenetic modifications at the consensus STAT3 binding site within the Gfap promoter, induces this pathological process. Furthermore, we demonstrated that the amniotic fluid exposure is the stimulator of STAT3 activation in MMC spinal cord NPCs, promoting GFAP expression and differentiation of NPCs into astrocytes. To validate this mechanism, we showed that elimination of Stat3 expression from NPCs using CRISPR/Cas9 inhibited GFAP expression and the emergence of astrocytes. Thus, our study provides a novel mechanism that drives abnormal astrogenesis in the developing MMC spinal cord.

Indexed as

AstrocytesEpigenesis, GeneticNeural Tube DefectsSTAT3 Transcription FactorAnimalsCell DifferentiationFemaleGlial Fibrillary Acidic ProteinNeural Stem CellsPregnancyRatsRats, Sprague-DawleySpinal CordGlial Fibrillary Acidic ProteinStat3 protein, ratSTAT3 Transcription FactorAmniotic fluidAstrocyte developmentMyelomeningoceleNeural tube defectsSTAT3

Identifiers

PMID40169106
PMCPMC12139518

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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.