Evidence map›Paper›PMID 37925518›Full record

ArticleScientific reports2023

Glutamate secretion by embryonic stem cells as an autocrine signal to promote proliferation.

Lin Teng, Qin Qin, Ziyi Zhou, Fei Zhou, Chunyu Cao, Jian Yang, Jiawang Ding

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

7 authors at 2 institutions in 1 country.

Lin TengDepartment of Cardiology, Yichang Central People's Hospital/The First College of Clinical Medical Sciences, China Three Gorges University, No. 183 Yiling Road, Yichang, 443003, Hubei, China.
Qin QinDepartment of Cardiology, Yichang Central People's Hospital/The First College of Clinical Medical Sciences, China Three Gorges University, No. 183 Yiling Road, Yichang, 443003, Hubei, China.
Ziyi ZhouDepartment of Cardiology, Yichang Central People's Hospital/The First College of Clinical Medical Sciences, China Three Gorges University, No. 183 Yiling Road, Yichang, 443003, Hubei, China.
Fei ZhouDepartment of Cardiology, Yichang Central People's Hospital/The First College of Clinical Medical Sciences, China Three Gorges University, No. 183 Yiling Road, Yichang, 443003, Hubei, China.
Chunyu CaoCollege of Basic Medical Sciences, Hubei Key Laboratory of Tumor Microencironment and Immunotherapy, China Three Gorges University, Yichang, 443000, Hubei, China.
Jian YangDepartment of Cardiology, Yichang Central People's Hospital/The First College of Clinical Medical Sciences, China Three Gorges University, No. 183 Yiling Road, Yichang, 443003, Hubei, China.
Jiawang DingDepartment of Cardiology, Yichang Central People's Hospital/The First College of Clinical Medical Sciences, China Three Gorges University, No. 183 Yiling Road, Yichang, 443003, Hubei, China. dingjiawang@163.com.
China Three Gorges University · CNYichang Central People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glutamate, the major excitatory neurotransmitter in the central nervous system, has also been found to play a role in embryonic stem (ES) cells. However, the exact mechanism and function of glutamatergic signaling in ES cells remain poorly understood. In this study, we identified a glutamatergic transmission circuit in ES cells that operates through an autocrine mechanism and regulates cell proliferation. We performed biological analyses to identify the key components involved in glutamate biosynthesis, packaging for secretion, reaction, and reuptake in ES cells, including glutaminase, vesicular glutamate transporter, glutamate N-methyl-D-aspartate (NMDA) receptor, and cell membrane excitatory amino-acid transporter (EAAT). We directly quantified the released glutamate signal using microdialysis-high performance liquid chromatography-tandem mass spectrometry (MD-HPLC-MS-MS). Pharmacological inhibition of endogenous glutamate release and the resulting tonic activation of NMDA receptors significantly affected ES cell proliferation, suggesting that ES cells establish a glutamatergic autocrine niche via releasing and responding to the transmitter for their own regulation.

Indexed as

Embryonic Stem CellsGlutamic AcidCell ProliferationExcitatory Amino AcidsReceptors, N-Methyl-D-AspartateExcitatory Amino AcidsGlutamic AcidReceptors, N-Methyl-D-Aspartate

Identifiers

PMID37925518
PMCPMC10625544
OpenAlexW4388340776

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.