Evidence map›Paper›PMID 33619902›Full record

ArticleOrthopaedic surgery2021

CircCDR1as Suppresses Bone Microvascular Endothelial Cell Activity and Angiogenesis Through Targeting miR-135b/ FIH-1 Axis.

Zheng Mao, Gang Liu, Gui-Yang Xiao, Chang Zhao, Yu-Cong Zou

Open access · goldAbstract read
In one paragraph

Article in Orthopaedic surgery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 32% 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, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Unique miRomics Expression Profiles inInternational journal of molecular sciences · 2023
    Article
  11. Article
  12. 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

5 authors at 2 institutions in 1 country.

Zheng MaoDepartment of Rehabilitation, The third Affiliated Hospital, Southern Medical University, Guangzhou, China.
Gang LiuDepartment of Rehabilitation, The third Affiliated Hospital, Southern Medical University, Guangzhou, China.
Gui-Yang XiaoHome for the Aged Guangzhou, Guangzhou, China.
Chang ZhaoDepartment of orthopedics, The Third affiliated hospital, Southern Medical University, Guangzhou, China.
Yu-Cong ZouDepartment of Rehabilitation, The third Affiliated Hospital, Southern Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0001-8678-2012
Third Affiliated Hospital of Southern Medical University · CNGuangzhou Experimental Station · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe current study investigated the role of CircCDR1as on angiogenesis of bone microvascular endothelial cells (BMECs) isolated from non-traumatic ONFH.

methodsForty corticosteroid-induced ONFH patients received THA were enrolled in our study. Expressions of CircCDR1as, miR-135b, and FIH-1 were detected by qRT-PCR in affected necrosis tissue and non-affected normal tissue. Bone microvascular endothelial cells (BMEC) were isolated from six patients and treated with 0.1 mg/mL hydrocortisone to establish a GC-damaged model of BMECs. Circ CDR1as plasmid and miR-135b mimic were transfected into BMECs. BMEC proliferation was assessed using MTT assays. The migration ability of cells was detected by scratch-wound assays. Matrigel assay was performed to detect angiogenesis in vitro. Western blot assay was used to detect HIF-1α, VEGF, and FIH-1 expressions. FISH, RNA pull down, RIP, and luciferase assay were carried out to determine the interaction of CircCDR1as, miR-135b, and FIH-1.

resultsCircCDR1as was upregulated(2.02 ± 0.30 vs. 1.00 ± 0.10,P < 0.001) whereas miR-135b was downregulated (0.55 ± 0.12 vs. 1.00 ± 0.10,P < 0.001) in affected tissues than in non-affected tissues. Expression of CircCDR1as and FIH-1 were negatively associated with miR-135b in affected tissues (CircCDR1as with miR-135b: r = -0.506, P < 0.001; FIH-1 with miR-135b r = -0.510, P < 0.001). Total blood tubule density was increased when CircCDR1as was silenced compared with NC (P < 0.01 vs. NC). The number of migrated BMECs were significantly increased in CircCDR1as silencing group compared with NC group (P < 0.05 vs. NC). In addition, CircCDR1as plasmids transfection increased the protein expressions of FIH-1 (P < 0.05 vs. NC) and reduced the HIF-1α as well as VEGF expression compared with NC group (P < 0.05 vs. NC). FISH, RNA pull down, RIP, and luciferase assay identified that FIH-1 was a target of miR-135b and could be modulated by CircCDR1as.

conclusionCircCDR1as decreases angiogenesis and proliferation of BMECs by sponging miR-135b and upregulate FIH-1.

Indexed as

Arthroplasty, Replacement, HipAngiogenesis Inducing AgentsApoptosisCell MovementCells, CulturedDown-RegulationEndothelial CellsFemur Head NecrosisHumansMicroRNAsMixed Function OxygenasesRepressor ProteinsRNA, Long NoncodingAngiogenesis Inducing AgentsHIF1AN protein, humanlong non-coding RNA CDR1AS, humanMicroRNAsMIRN135 microRNA, humanMixed Function OxygenasesRepressor ProteinsRNA, Long NoncodingAngiogenesisBone microvascular endothelial cellsCompeting endogenous RNAsNon-traumatic osteonecrosis of femoral head

Identifiers

PMID33619902
PMCPMC7957389
OpenAlexW3132303172

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.