Evidence map›Paper›PMID 32562373›Full record

ArticleJournal of cellular and molecular medicine2020

MiR-155 promotes interleukin-1β-induced chondrocyte apoptosis and catabolic activity by targeting PIK3R1-mediated PI3K/Akt pathway.

Zhiyong Fan, Yinghui Liu, Zhengliang Shi, Kai Deng, Hua Zhang, Qiutong Li, Shuxing Cao, Shentai Li, Hongliang Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

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  18. Crosstalk Among circRNA/lncRNA, miRNA, and mRNA in Osteoarthritis.Frontiers in cell and developmental biology · 2021
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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

9 authors at 1 institution in 1 country.

Zhiyong FanDepartment of Orthopaedic Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Yinghui LiuDepartment of Infectious Disease, The Third Hospital of Hebei Medical University, Shijiazhuang, China.
Zhengliang ShiDepartment of Orthopaedic Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Kai DengDepartment of Orthopaedic Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Hua ZhangDepartment of Orthopaedic Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, China.ORCID 0000-0002-6714-0847
Qiutong LiDepartment of Orthopaedic Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Shuxing CaoDepartment of Orthopaedic Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Shentai LiDepartment of Orthopaedic Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Hongliang ZhangDepartment of Orthopaedic Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) is a common joint disease characterized by progressive cartilage degradation, in which elevated chondrocyte apoptosis and catabolic activity play an important role. MicroRNA-155 (miR-155) has recently been shown to regulate apoptosis and catabolic activity in some pathological circumstances, yet, whether and how miR-155 is associated with OA pathology remain unexplored. We report here that miR-155 level is significantly up-regulated in human OA cartilage biopsies and also in primary chondrocytes stimulated by interleukin-1β (IL-1β), a pivotal pro-catabolic factor promoting cartilage degradation. Moreover, miR-155 inhibition attenuates and its overexpression promotes IL-1β-induced apoptosis and catabolic activity in chondrocytes in vitro. We also demonstrate that the PIK3R1 (p85α regulatory subunit of phosphoinositide 3-kinase (PI3K)) is a target of miR-155 in chondrocytes, and more importantly, PIK3R1 restoration abrogates miR-155 effects on chondrocyte apoptosis and catabolic activity. Mechanistically, PIK3R1 positively regulates the transduction of PI3K/Akt pathway, and a specific Akt inhibitor reverses miR-155 effects on promoting chondrocyte apoptosis and catabolic activity, phenocopying the results obtained via PIK3R1 knockdown, hence establishing that miR-155 promotes chondrocyte apoptosis and catabolic activity through targeting PIK3R1-mediated PI3K/Akt pathway activation. Altogether, our study discovers novel roles and mechanisms of miR-155 in regulating chondrocyte apoptosis and catabolic activity, providing an implication for therapeutically intervening cartilage degradation and OA progression.

Indexed as

ApoptosisCartilageCells, CulturedChondrocytesClass Ia Phosphatidylinositol 3-KinaseExtracellular MatrixHumansInterleukin-1betaMicroRNAsOsteoarthritisPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionClass Ia Phosphatidylinositol 3-KinaseIL1B protein, humanInterleukin-1betaMicroRNAsMIRN155 microRNA, humanPhosphatidylinositol 3-KinasesPIK3R1 protein, humanProto-Oncogene Proteins c-aktapoptosiscatabolic activitychondrocyteMiR-155osteoarthritisPIK3R1

Identifiers

PMID32562373
PMCPMC7412691
OpenAlexW3036954831

What Socratic 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 Socratic graph.