Evidence map›Paper›PMID 33522639›Full record

ArticleCell proliferation2021

CTGF facilitates cell-cell communication in chondrocytes via PI3K/Akt signalling pathway.

Zuping Wu, Chenchen Zhou, Quan Yuan, Demao Zhang, Jing Xie, Shujuan Zou

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 51 citations in OpenAlex.

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  11. Connective Tissue Growth Factor: Regulation, Diseases, and Drug Discovery.International journal of molecular sciences · 2024
    Review
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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

6 authors at 1 institution in 1 country.

Zuping WuState Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Chenchen ZhouState Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Quan YuanState Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.ORCID https://orcid.org/0000-0002-2836-1081
Demao ZhangState Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Jing XieState Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.ORCID https://orcid.org/0000-0001-8156-0322
Shujuan ZouState Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Sichuan University · CN

Funding

National Natural Science Foundation of China 81600840National Natural Science Foundation of China 81771047
6 · The paper itself

Abstract

purposesGap junction intercellular communication (GJIC) is essential for articular cartilage to respond appropriately to physical or biological stimuli and maintain homeostasis. Connective tissue growth factor (CTGF), identified as an endochondral ossification genetic factor, plays a vital role in cell proliferation, migration and adhesion. However, how CTGF regulates GJIC in chondrocytes is still unknown. This study aims to explore the effects of CTGF on GJIC in chondrocytes and its potential biomechanism. MATERIALS AND

methodsqPCR was performed to determine the expression of gene profile in the CCN family in chondrocytes. After CTGF treatment, CCK-8 assay and scratch assay were performed to explore cell proliferation and migration. A scrape loading/dye transfer assay was adopted to visualize GJIC in living chondrocytes. Western blot analysis was done to detect the expression of Cx43 and PI3K/Akt signalling. Immunofluorescence staining was used to show protein distribution. siRNA targeting CTGF was used to detect the influence on cell-cell communication.

resultsThe CTGF (CCN2) was shown to be the highest expressed member of the CCN family in chondrocytes. CTGF facilitated functional gap junction intercellular communication in chondrocytes through up-regulation of Cx43 expressions. CTGF activated PI3K/Akt signalling to promote Akt phosphorylation and translocation. Suppressing CTGF also reduced the expression of Cx43. The inhibition of PI3K/Akt signalling decreased the expressions of Cx43 and thus impaired gap junction intercellular communication enhanced by CTGF.

conclusionsFor the first time, we provide evidence to show CTGF facilitates cell communication in chondrocytes via PI3K/Akt signalling pathway.

Indexed as

Signal TransductionAnimalsCartilage, ArticularCell CommunicationCell ProliferationChondrocytesGap JunctionsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktchondrocytesConnexin43CTGFgap junction intercellular communication

Identifiers

PMID33522639
PMCPMC7941231
OpenAlexW3128056238

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.