Evidence map›Paper›PMID 34350461›Full record

ArticleBioscience reports2021

Parathyroid hormone promotes the osteogenesis of lipopolysaccharide-induced human bone marrow mesenchymal stem cells through the JNK MAPK pathway.

Ziyue Qin, Shu Hua, Huifen Chen, Zhuo Wang, Haoran Wang, Jiamin Xu, Yuli Wang, Wu Chen, Weina Zhou

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

Article in Bioscience reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

9 authors at 1 institution in 1 country.

Ziyue Qin *Department of Periodontology, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China.ORCID 0000-0002-1520-8272
Shu Hua *Jiangsu Province Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Huifen ChenJiangsu Province Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Zhuo WangJiangsu Province Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Haoran WangJiangsu Province Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Jiamin XuJiangsu Province Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Yuli WangJiangsu Province Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.ORCID 0000-0002-5500-3351
Wu ChenDepartment of Periodontology, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China.
Weina ZhouJiangsu Province Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Periodontitis is a series of inflammatory processes caused by bacterial infection. Parathyroid hormone (PTH) plays a critical role in bone remodeling. The present study aimed to investigate the influences of PTH on human bone marrow mesenchymal stem cells (HBMSCs) pretreated with lipopolysaccharide (LPS). The proliferative ability was measured using cell counting kit-8 (CCK-8) and flow cytometry. The optimal concentrations of PTH and LPS were determined using alkaline phosphatase (ALP) activity assay, ALP staining, and Alizarin Red staining. Osteogenic differentiation was further assessed by quantitative reverse-transcription polymerase chain reaction (RT-qPCR), Western blot analysis, and immunofluorescence staining. PTH had no effects on the proliferation of HBMSCs. Also, 100 ng/ml LPS significantly inhibited HBMSC osteogenesis, while 10-9 mol/l PTH was considered as the optimal concentration to reverse the adverse effects. Mechanistically, c-Jun N-terminal kinase (JNK) phosphorylation was activated by PTH in LPS-induced HBMSCs. SP600125, a selective inhibitor targeting JNK mitogen-activated protein kinase (MAPK) signaling, weakened the effects of PTH. Taken together, the findings revealed the role and mechanism of PTH and JNK pathway in promoting the osteogenic differentiation of LPS-induced HBMSCs, which offered an alternative for treating periodontal diseases.

Indexed as

AdultCell DifferentiationCells, CulturedHumansJNK Mitogen-Activated Protein KinasesLipopolysaccharidesMesenchymal Stem CellsOsteogenesisParathyroid HormonePeriodontitisPhosphorylationSignal TransductionYoung AdultJNK Mitogen-Activated Protein KinasesLipopolysaccharidesParathyroid HormonePTH protein, humanHuman bone marrow mesenchymal stem cellsLipopolysaccharidesMitogen-activated protein kinase signaling pathwayOsteogenic differentiationParathyroid hormone

Identifiers

PMID34350461
PMCPMC8380916
OpenAlexW3189593215

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.