Evidence map›Paper›PMID 31111299›Full record

ArticleInflammation2019

TNF-α Regulates ITGβ1 and SYND4 Expression in Nucleus Pulposus Cells: Activation of FAK/PI3K Signaling.

Xinghuo Wu, Suyun Li, Kun Wang, Wenbin Hua, Shuai Li, Yu Song, Yukun Zhang, Shuhua Yang, Cao Yang

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 13 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

9 authors at 2 institutions in 1 country.

Xinghuo WuDepartment of Orthopaedic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei, China.
Suyun LiDepartment of Orthopaedic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei, China.
Kun WangDepartment of Orthopaedic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei, China.
Wenbin HuaDepartment of Orthopaedic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei, China.
Shuai LiDepartment of Orthopaedic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei, China.
Yu SongDepartment of Orthopaedic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei, China.
Yukun ZhangDepartment of Orthopaedic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei, China.
Shuhua YangDepartment of Orthopaedic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei, China.
Cao YangDepartment of Orthopaedic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei, China. yangcao1971@sina.com.
Union Hospital · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Integrins can function synergistically with syndecan-4 (SYND4) and bind to the fibronectin (FN) matrix, resulting in the regulation of tissue regeneration. This study aimed to explore the effects of TNF-α on the formation of FN/ITGβ1/SYND4 complex and the relative mechanism in NP cells. The expression of FN-ITG-SYND4 at the cellular level under TNF-α stimulation was detected by immunofluorescent staining, western blotting, and RT-PCR. ITGβ1 is a crucial component of ITG FN-induced FAK signaling, which was detected using dual mode. And, the involved signaling down stream pathways were also detected. FN is a preferred adhesion substrate for NP cells and that integrin β1 (ITGβ1) and SYND4 work synergistically during ECM engagement in a focal adhesion kinase (FAK)-dependent fashion. The PI3k/Akt pathway is obviously down-regulated, resulting in decreased adherence capacity and increased anoikis. TNF-α induction could weaken FAK activity and downstream levels of phospho-PI3K and Akt, resulting in decreased adherence capacity and increased apoptosis. Thus, TNF-α is essential for the formation of FN/ITGβ1/SYND4 complex in NP cells and further elucidates the inflammatory mechanism of NP cells degeneration.

Indexed as

Cell AdhesionCells, CulturedExtracellular MatrixFibronectinsFocal Adhesion Protein-Tyrosine KinasesHumansIntegrin beta1Nucleus PulposusPhosphatidylinositol 3-KinasesSignal TransductionSyndecan-4Tumor Necrosis Factor-alphaFibronectinsFocal Adhesion Protein-Tyrosine KinasesIntegrin beta1Phosphatidylinositol 3-KinasesSyndecan-4Tumor Necrosis Factor-alphaadhesionanoikisdegenerationfibronectinintegrinsintervertebral disc

Identifiers

PMID31111299
OpenAlexW2945973743

What Socratic 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 Socratic graph.