Evidence map›Paper›PMID 37556489›Full record

ArticlePloS one2023

Sp1 mediated the inhibitory effect of glutamate on pulmonary surfactant synthesis.

Xiao-Hong Li, Jie-Jun Fu, Xiao-Juan Shi, Yun-Na Zhang, Min Shao, Shao-Jie Yue, Chen Li, Zi-Qiang Luo

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2023. 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
0.8field-weighted citation impact, top 24% 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, 3 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

8 authors at 1 institution in 1 country.

Xiao-Hong LiDepartment of Pathology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jie-Jun FuDepartment of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
Xiao-Juan ShiDepartment of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
Yun-Na ZhangDepartment of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
Min ShaoDepartment of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
Shao-Jie YueDepartment of Pediatrics, Xiangya Hospital, Central South University, Changsha, China.
Chen LiDepartment of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China.ORCID 0000-0002-0905-4297
Zi-Qiang LuoDepartment of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China.ORCID 0000-0002-3808-6159
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundStudies have shown that the release of endogenous glutamate (Glu) participates in lung injury by activating N-methyl-D-aspartate receptor (NMDAR), but the mechanism is still unclear. This study was to investigate the effects and related mechanisms of Glu on the lipid synthesis of pulmonary surfactant (PS) in isolated rat lung tissues.

methodsThe cultured lung tissues of adult SD rats were treated with Glu. The amount of [3H]-choline incorporation into phosphatidylcholine (PC) was detected. RT-PCR and Western blot were used to detect the changes of mRNA and protein expression of cytidine triphosphate: phosphocholine cytidylyltransferase alpha (CCTα), a key regulatory enzyme in PC biosynthesis. Western blot was used to detect the expression of NMDAR1, which is a functional subunit of NMDAR. Specific protein 1 (Sp1) expression plasmids were used. After transfected with Sp1 expression plasmids, the mRNA and protein levels of CCTα were detected by RT-PCR and Western blot in A549 cells. After treated with NMDA and MK-801, the mRNA and protein levels of Sp1 were detected by RT-PCR and Western blot in A549 cells.

resultsGlu decreased the incorporation of [3H]-choline into PC in a concentration- and time- dependent manner. Glu treatment significantly reduced the mRNA and protein levels of CCTα in lungs. Glu treatment up-regulated NMDAR1 protein expression, and the NMDAR blocker MK-801 could partially reverse the reduction of [3H]-choline incorporation induced by Glu (10-4 mol/L) in lungs. After transfected with Sp1 plasmid for 30 h, the mRNA and protein expression levels of CCTα were increased and the protein expression of Sp1 was also up-regulated. After A549 cells were treated with NMDA, the level of Sp1 mRNA did not change significantly, but the expression of nucleus protein in Sp1 was significantly decreased, while the expression of cytoplasmic protein was significantly increased. However, MK-801could reverse these changes.

conclusionsGlu reduced the biosynthesis of the main lipid PC in PS and inhibited CCTα expression by activating NMDAR, which were mediated by the inhibition of the nuclear translocation of Sp1 and the promoter activity of CCTα. In conclusion, NMDAR-mediated Glu toxicity leading to impaired PS synthesis may be a potential pathogenesis of lung injury.

Indexed as

Lung InjuryPulmonary SurfactantsSp1 Transcription FactorAnimalsCholineCholine-Phosphate CytidylyltransferaseDizocilpine MaleateGlutamic AcidN-MethylaspartatePhosphatidylcholinesRatsRats, Sprague-DawleyRNA, MessengerCholineCholine-Phosphate CytidylyltransferaseDizocilpine MaleateGlutamic AcidN-MethylaspartatePhosphatidylcholinesPulmonary SurfactantsRNA, MessengerSp1 Transcription Factor

Identifiers

PMID37556489
PMCPMC10411742
OpenAlexW4385694022

What OpenQuestion 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 OpenQuestion graph.