Evidence map›Paper›PMID 26573126›Full record

ArticleMolecular medicine reports2016

Microfluidics‑based optimization of neuroleukin‑mediated regulation of articular chondrocyte proliferation.

Kang Tian, Weiliang Zhong, Yingqiu Zhang, Baosheng Yin, Weiguo Zhang, Han Liu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

6 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
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 2 institutions in 1 country.

Kang TianDepartment of Orthopaedics, First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning 116044, P.R. China.
Weiliang ZhongDepartment of Orthopaedics, First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning 116044, P.R. China.
Yingqiu ZhangDepartment of Orthopaedics, First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning 116044, P.R. China.
Baosheng YinDepartment of Orthopaedics, First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning 116044, P.R. China.
Weiguo ZhangDepartment of Orthopaedics, First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning 116044, P.R. China.
Han LiuDepartment of Orthopaedics, First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning 116044, P.R. China.
Dalian Medical University · CNFirst Affiliated Hospital of Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Due to the low proliferative and migratory capacities of chondrocytes, cartilage repair remains a challenging clinical problem. Current therapeutic strategies for cartilage repair result in unsatisfactory outcomes. Autologous chondrocyte implantation (ACI) is a cell based therapy that relies on the in vitro expansion of healthy chondrocytes from the patient, during which proliferation‑promoting factors are frequently used. Neuroleukin (NLK) is a multifunctional protein that possesses growth factor functions, and its expression has been associated with cartilage development and bone regeneration, however its direct role in chondrocyte proliferation remains to be fully elucidated. In the current study, the role of NLK in chondrocyte proliferation in vitro in addition to its potential to act as an exogenous factor during ACI was investigated. Furthermore, the concentration of NLK for in vitro chondrocyte culture was optimized using a microfluidic device. An NLK concentration of 12.85 ng/ml was observed to provide optimal conditions for the promotion of chondrocyte proliferation. Additionally, NLK stimulation resulted in an increase in type II collagen synthesis by chondrocytes, which is a cartilaginous secretion marker and associated with the phenotype of chondrocytes. Together these data suggest that NLK is able to promote cell proliferation and type II collagen synthesis during in vitro chondrocyte propagation, and thus may serve as an exogenous factor for ACI.

Indexed as

AnimalsCartilage, ArticularCell ProliferationCells, CulturedCell ShapeChondrocytesCollagen Type IICytokinesEquipment DesignGlucose-6-Phosphate IsomeraseMaleMicrofluidicsRats, Sprague-DawleyReproducibility of ResultsCollagen Type IICytokinesGlucose-6-Phosphate IsomeraseGPI protein, human

Identifiers

PMID26573126
PMCPMC4686044
OpenAlexW2148663129

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.