Evidence map›Paper›PMID 31496660›Full record

ArticleDrug design, development and therapy2019

Overexpression of SOX9 alleviates the progression of human osteoarthritis in vitro and in vivo.

Yuanming Ouyang, Wei Wang, Bing Tu, Yi Zhu, Cunyi Fan, Yanfeng Li

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

Article in Drug design, development and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 65 citations in OpenAlex.

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  18. Healthy and Osteoarthritis-Affected Joints Facing the Cellular Crosstalk.International journal of molecular sciences · 2023
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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 3 institutions in 1 country.

Yuanming OuyangDepartment of Orthopedics, Shanghai Sixth People's Hospital East Campus Shanghai University of Medicine and Health, Shanghai 201306, People's Republic of China.
Wei WangDepartment of Orthopedics, Shanghai Sixth People's Hospital East Campus Shanghai University of Medicine and Health, Shanghai 201306, People's Republic of China.
Bing TuDepartment of Orthopedics, Shanghai Sixth People's Hospital East Campus Shanghai University of Medicine and Health, Shanghai 201306, People's Republic of China.
Yi ZhuDepartment of Orthopedics, Shanghai Sixth People's Hospital East Campus Shanghai University of Medicine and Health, Shanghai 201306, People's Republic of China.
Cunyi FanDepartment of Orthopedics, Shanghai Sixth People's Hospital East Campus Shanghai University of Medicine and Health, Shanghai 201306, People's Republic of China.
Yanfeng LiDepartment of Orthopedics, Shanghai Sixth People's Hospital East Campus Shanghai University of Medicine and Health, Shanghai 201306, People's Republic of China.
Shanghai University · CNShanghai Sixth People's Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeRecent findings have identified that SOX9 served as a key role during the pathogenesis of osteoarthritis (OA). This study aimed to investigate the mechanisms by which SOX9 regulated the formation of OA in vitro and in vivo. MATERIALS AND

methodsThe relative expressions of SOX9 in patients with OA and normal fracture of thighbone were analyzed by real-time-PCR. In vitro, IL-1β induced inflammatory response in human chondrocytes was used to evaluate the function of SOX9. The recombinant SOX9 lentivirus vector (Lenti-SOX9) was used to upregulate the expression of SOX9 in cells. ELISA was used to measure the concentration of tumor necrosis factor-α (TNF-α). The protein expressions of SOX9, matrix metalloproteinase-13 (MMP13), Collagen II, Aggrecan and Smad3 were analyzed by Western blot. Cell proliferation and cell apoptosis were detected by CCK-8 assay and flow cytometry, respectively. In vivo, the effect of SOX9 on surgically induced OA mice was evaluated.

resultsThe gene level of SOX9 was remarkably downregulated in patients with OA compared with normal people, while the concentration of TNF-α was upregulated. In addition, IL-1β reduced the expressions of SOX9, Collagen II and Aggrecan and increased the level of MMP13 in chondrocytes. Moreover, Lenti-SOX9 notably inhibited IL-1β-induced growth inhibition and apoptosis in chondrocytes via increasing the expression of Smad3. Finally, Lenti-SOX9 markedly alleviated the symptoms of OA mice in vivo.

conclusionUpregulation of SOX9 inhibited IL-1β-induced inflammatory response via increasing the level Smad3 in human chondrocytes and exhibited therapeutic effect on surgically induced OA mice in vivo. Therefore, SOX9 may serve as a potential target in the treatment of OA in the future.

Indexed as

AnimalsCells, CulturedDisease Models, AnimalDisease ProgressionHumansMaleMiceMice, Inbred C57BLOsteoarthritisSOX9 Transcription FactorSOX9 protein, humanSOX9 Transcription FactorcollagenIL-1βinflammationosteoarthritisSOX9

Identifiers

PMID31496660
PMCPMC6698167
OpenAlexW2981849589

What OpenQuestion holds

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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.