Evidence map›Paper›PMID 39604981›Full record

ArticleCell communication and signaling : CCS2024

Chondroprotective functions of neutrophil-derived extracellular vesicles by promoting the production of secreted frizzled-related protein 5 in cartilage.

Keita Kitahara, Taku Ebata, Chen Liyile, Yoshio Nishida, Yuki Ogawa, Taiki Tokuhiro, Junki Shiota, Tatsuya Nagano, Taichi E Takasuka, Tsutomu Endo and 9 more

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

8 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. 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

19 authors.

Keita KitaharaDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Taku EbataDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Chen LiyileDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Yoshio NishidaDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Yuki OgawaDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Taiki TokuhiroDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Junki ShiotaDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Tatsuya NaganoResearch Faculty of Agriculture, Hokkaido University, Kita-9, Nishi-9, Kitaku, Sapporo, 060-8589, Japan.
Taichi E TakasukaResearch Faculty of Agriculture, Hokkaido University, Kita-9, Nishi-9, Kitaku, Sapporo, 060-8589, Japan.
Tsutomu EndoDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Tomohiro ShimizuDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Hend AlhasanDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Tsuyoshi AsanoDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Daisuke TakahashiDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Kentaro HomanDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Tomohiro OnoderaDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Ken KadoyaDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
M Alaa TerkawiDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan. materkawi@med.hokudai.ac.jp.
Norimasa IwasakiDepartment of Orthopedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.

Funding

Japan Agency for Medical Research and Development PJ4221KB01Japan Society for the Promotion of Science (Grant-in-Aid for Scientific Research C) 20K09471
6 · The paper itself

Abstract

backgroundOsteoarthritis (OA) is the most common degenerative joint disease characterized by cartilage degradation and various degrees of inflammation in the synovium. Growing evidence highlights that neutrophil extracellular vesicles (EVs) play a protective role in arthritic joints by promoting the resolution of inflammation and the synthesis of proteoglycans in cartilage. However, this homeostatic function is dependent on the activation state of neutrophils and the surrounding environment/tissues. Hence, we explored the chondroprotective functions of neutrophil-derived EVs under different stimulation conditions and the underlying molecular mechanism.

methodsHuman blood-derived neutrophils, murine bone marrow-derived neutrophils, C-28I2 cells and primary chondrocytes were used. Neutrophils were stimulated with different cytokines, and their EVs were isolated for chondrocyte stimulation and further subjected to RNA-sequencing analysis. Two experimental murine OA models were used, and the treatment was performed by intraarticular injections.

resultsConditioned medium from neutrophils stimulated with TGF-β (N-β) had the greatest inhibitory effect on the expression of catabolic factors in stimulated chondrocytes. These protective effects were not impaired when conditioned medium of N-β from AnxA1-deficient mice was used. Consistent with these results, EVs isolated from N-β significantly reduced the expression of catabolic factors in stimulated chondrocytes. Bulk RNA-seq analysis revealed that secreted frizzled-related protein 5 (SFRP5) is upregulated in N-β-EV-stimulated chondrocytes. Furthermore, recombinant SFRP5 treatment significantly reduced the expression of catabolic factors in vitro and catabolic process in experimental murine OA models.

conclusionsThe current study emphasizes the potential therapeutic application of neutrophils in OA and provides new knowledge on the molecular mechanisms underlying their function.

Indexed as

ChondrocytesExtracellular VesiclesNeutrophilsAnimalsCartilageCartilage, ArticularCulture Media, ConditionedDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLOsteoarthritisTransforming Growth Factor betaCulture Media, ConditionedTransforming Growth Factor beta

Identifiers

PMID39604981
PMCPMC11603793

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Registered trials

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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.