Evidence map›Paper›PMID 38123662›Full record

ArticleScientific reports2023

HOXA10 promotes Gdf5 expression in articular chondrocytes.

Tomohiko Murakami, Lerdluck Ruengsinpinya, Yoshifumi Takahata, Yuri Nakaminami, Kenji Hata, Riko Nishimura

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. 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 2 countries.

Tomohiko Murakami *Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamada-Oka, Suita, Osaka, 565-0871, Japan. murakami.tomohiko.dent@osaka-u.ac.jp.
Lerdluck Ruengsinpinya *Department of Oral Surgery and Oral Medicine, Faculty of Dentistry, Srinakharinwirot University, Bangkok, 10110, Thailand.
Yoshifumi Takahata *Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamada-Oka, Suita, Osaka, 565-0871, Japan.
Yuri NakaminamiDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamada-Oka, Suita, Osaka, 565-0871, Japan.
Kenji HataDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamada-Oka, Suita, Osaka, 565-0871, Japan.
Riko NishimuraDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamada-Oka, Suita, Osaka, 565-0871, Japan. nishimura.riko.dent@osaka-u.ac.jp.
Osaka University · JPSrinakharinwirot University · TH

Funding

Japan Society for the Promotion of Science JP16H06393Japan Society for the Promotion of Science JP22H03261
6 · The paper itself

Abstract

Growth differentiation factor 5 (GDF5), a BMP family member, is highly expressed in the surface layer of articular cartilage. The GDF5 gene is a key risk locus for osteoarthritis and Gdf5-deficient mice show abnormal joint development, indicating that GDF5 is essential in joint development and homeostasis. In this study, we aimed to identify transcription factors involved in Gdf5 expression by performing two-step screening. We first performed microarray analyses to find transcription factors specifically and highly expressed in the superficial zone (SFZ) cells of articular cartilage, and isolated 11 transcription factors highly expressed in SFZ cells but not in costal chondrocytes. To further proceed with the identification, we generated Gdf5-HiBiT knock-in (Gdf5-HiBiT KI) mice, by which we can easily and reproducibly monitor Gdf5 expression, using CRISPR/Cas9 genome editing. Among the 11 transcription factors, Hoxa10 clearly upregulated HiBiT activity in the SFZ cells isolated from Gdf5-HiBiT KI mice. Hoxa10 overexpression increased Gdf5 expression while Hoxa10 knockdown decreased it in the SFZ cells. Moreover, ChIP and promoter assays proved the direct regulation of Gdf5 expression by HOXA10. Thus, our results indicate the important role played by HOXA10 in Gdf5 regulation and the usefulness of Gdf5-HiBiT KI mice for monitoring Gdf5 expression.

Indexed as

Cartilage, ArticularOsteoarthritisAnimalsChondrocytesGrowth Differentiation Factor 5Homeobox A10 ProteinsMiceTranscription FactorsGdf5 protein, mouseGrowth Differentiation Factor 5Homeobox A10 ProteinsHoxa10 protein, mouseTranscription Factors

Identifiers

PMID38123662
PMCPMC10733362
OpenAlexW4389992433

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.