Evidence map›Paper›PMID 27376650›Full record

ArticleCytotechnology2016

The role of oncostatin M regulates osteoblastic differentiation of dental pulp stem cells through STAT3 pathway.

Xingmei Feng, Shuling Shen, Peipei Cao, Linhe Zhu, Ye Zhang, Ke Zheng, Guijuan Feng, Dongmei Zhang

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

Article in Cytotechnology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 19 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

8 authors at 3 institutions in 1 country.

Xingmei FengDepartment of Stomatology, Affiliated Hospital of Nantong University, Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong, 226000, China.
Shuling ShenDepartment of Stomatology, Affiliated Hospital of Nantong University, Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong, 226000, China.
Peipei CaoDepartment of Stomatology, Affiliated Hospital of Nantong University, Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong, 226000, China.
Linhe ZhuDepartment of Mathematics, Nanjing University of Aeronautics and Astronautics, Nanjing, 210016, China.
Ye ZhangDepartment of Stomatology, Affiliated Hospital of Nantong University, Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong, 226000, China.
Ke ZhengDepartment of Stomatology, Affiliated Hospital of Nantong University, Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong, 226000, China.
Guijuan FengDepartment of Stomatology, Affiliated Hospital of Nantong University, Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong, 226000, China. fengguijuan2013@126.com.
Dongmei ZhangDepartment of Pathogen Biology, Medical College, Nantong University, Nantong, 226000, China. zdm060608@163.com.
Nantong University · CNAffiliated Hospital of Nantong University · CNNanjing University of Aeronautics and Astronautics · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dental pulp stem cells (DPSCs) are a type of mesenchymal stem cells, which have the self-renewal and multi-lineage differentiation potential, including chondrocytes, adipocytes, neural cells and osteoblasts. So they play a significant role in pulp repair and bone regeneration. Oncostatin M (OSM), one of the IL-6 family cytokines, inhibits adipogenic differentiation and stimulates osteogenic differentiation of human bone marrow mesenchymal stem cells. However, the effect of OSM on DPSCs is unclear. We found that OSM induced osteogenic differentiation of DPSCs, promoting matrix mineralization as measured by Alizarin Red S staining. OSM also increased expression of osteogenesis-associated gene products Alkaline phosphatase, Bone morphogenetic protein 2 (BMP2), Runt-related transcription factor 2 and Osteocalcin (OCN) as assessed by immunoblotting. We also found that OSM activated the Signal Transducer And Activator Of Transcription 3 (STAT3) pathway during the osteogenic differentiation of DPSCs. Blocking the osteogenic differentiation by silencing of STAT3 can significantly inhibit OSM-induced osteogenic differentiation of DPSCs and the expression of related genes, furthermore matrix mineralization was also suppressed. In summary, OSM promotes osteoblastic differentiation of DPSCs and osteogenesis-related genes expression through the JAK3/STAT3 signaling pathway which may be useful for the autologous transplantation of DPSCs.

Indexed as

Dental pulp stem cells (DPSCs)Janus kinase 3 (JAK3)OSMOsteogenic differentiationSTAT3

Identifiers

PMID27376650
PMCPMC5101341
OpenAlexW2474448888

What OpenQuestion 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 OpenQuestion graph.