Evidence map›Paper›PMID 29843768›Full record

ArticleJournal of orthopaedic surgery and research2018

Egr-1 increases angiogenesis in cartilage via binding Netrin-1 receptor DCC promoter.

Jun Sheng, Da Liu, Xia Kang, Ying Chen, Kai Jiang, Wei Zheng

Open access · goldAbstract read
In one paragraph

Article in Journal of orthopaedic surgery and research, 2018. 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
2.0field-weighted citation impact, top 14% 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, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. EGR1 Enhances Lymphangiogenesis via SOX18-Mediated Activation of JAK2/STAT3 Pathway.Computational and mathematical methods in medicine · 2022
    Article
  8. Article
  9. Review
  10. Frontiers in genetics · 2021
    Article
  11. Review
  12. 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

6 authors at 1 institution in 1 country.

Jun ShengDepartment of Orthopedics, Chengdu Military General Hospital, 270 Rongdu Avenue, Jinniu District, Chengdu, 610083, Sichuan, China.
Da LiuDepartment of Orthopedics, Chengdu Military General Hospital, 270 Rongdu Avenue, Jinniu District, Chengdu, 610083, Sichuan, China.
Xia KangDepartment of Orthopedics, Chengdu Military General Hospital, 270 Rongdu Avenue, Jinniu District, Chengdu, 610083, Sichuan, China.
Ying ChenDepartment of Orthopedics, Chengdu Military General Hospital, 270 Rongdu Avenue, Jinniu District, Chengdu, 610083, Sichuan, China.
Kai JiangDepartment of Orthopedics, Chengdu Military General Hospital, 270 Rongdu Avenue, Jinniu District, Chengdu, 610083, Sichuan, China.
Wei ZhengDepartment of Orthopedics, Chengdu Military General Hospital, 270 Rongdu Avenue, Jinniu District, Chengdu, 610083, Sichuan, China. zhengweipaper@sina.com.
Chengdu Military General Hospital · CN

Funding

Department of Science and Technology of Sichuan Province 2014JY0009
6 · The paper itself

Abstract

backgroundOsteoarthritis (OA) is a joint disease characterized by degradation of cartilage. The etiology of OA is still unclear. Vascular endothelial growth factor (VEGF) plays a key role of angiogenesis in the pathogenesis of OA and contributes to the angiogenesis of NT-1/DCC. Whether or not NT-1/DCC and VEGF interact in regulating angiogenesis of OA cartilage is not known.

methodsHistological studies for CD34, VEGF, and safranin-O staining were performed to determine angiogenesis and cartilage tissue injury. ELISA indicated the level of pro-inflammation cytokines. Immunoblotting, immunoprecipitation, and electrophoretic mobility shift assay (EMSA) were performed to assay the expression and function of NT-1/DCC-VEGF signaling pathway.

resultsOur data indicated that VEGF expression was increased in cartilage tissue from OA rats, while the chondrocytes were disorganized, and cartilage degeneration was increasing in OA rats. The inflammation factors in articular cavity fluid were higher in the OA rats than in the sham. The protein expression of NT-1, DCC, and VEGF were increased in osteoarthritic cartilage. DCC was involved in the positive regulation of osteoarthritic angiogenesis by VEGF. Egr-1 expression was higher in OA rats than in sham rats. Egr-1 is a regulator of DCC promoter activity, and the binding is higher in OA rats than in sham rats.

conclusionOur present study provides a mechanism by which Egr-1 induced angiogenesis via NT-1/DCC-VEGF pathway.

Indexed as

Angiogenesis Inducing AgentsAnimalsCartilageDCC ReceptorEarly Growth Response Protein 1Netrin ReceptorsOsteoarthritisPromoter Regions, GeneticProtein BindingRatsRats, Inbred LewAngiogenesis Inducing AgentsDcc protein, ratDCC ReceptorEarly Growth Response Protein 1Egr1 protein, ratNetrin ReceptorsAngiogenesisDDC promoterEgr-1Netrin-1 receptorOsteoarthritis

Identifiers

PMID29843768
PMCPMC5975438
OpenAlexW2805436872

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.