Evidence map›Paper›PMID 38704516›Full record

ArticleJournal of bone and mineral metabolism2024

Plasminogen activator inhibitor-1 is involved in glucocorticoid-induced decreases in angiogenesis during bone repair in mice.

Kiyotaka Okada, Yuto Niwa, Kazusa Fukuhara, Takashi Ohira, Yuya Mizukami, Naoyuki Kawao, Osamu Matsuo, Hiroshi Kaji

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of bone and mineral metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. 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

8 authors.

Kiyotaka OkadaDepartment of Arts and Science, Faculty of Medicine, Kindai University, 377-2 Ohno-Higashi, Osakasayama, Osaka, 589-8511, Japan.
Yuto NiwaDepartment of Physiology and Regenerative Medicine, Faculty of Medicine, Kindai University, 377-2 Ohno-Higashi, Osakasayama, Osaka, 589-8511, Japan.
Kazusa FukuharaDepartment of Physiology and Regenerative Medicine, Faculty of Medicine, Kindai University, 377-2 Ohno-Higashi, Osakasayama, Osaka, 589-8511, Japan.
Takashi OhiraDepartment of Physiology and Regenerative Medicine, Faculty of Medicine, Kindai University, 377-2 Ohno-Higashi, Osakasayama, Osaka, 589-8511, Japan.
Yuya MizukamiDepartment of Physiology and Regenerative Medicine, Faculty of Medicine, Kindai University, 377-2 Ohno-Higashi, Osakasayama, Osaka, 589-8511, Japan.
Naoyuki KawaoDepartment of Physiology and Regenerative Medicine, Faculty of Medicine, Kindai University, 377-2 Ohno-Higashi, Osakasayama, Osaka, 589-8511, Japan.
Osamu MatsuoDepartment of Physiology and Regenerative Medicine, Faculty of Medicine, Kindai University, 377-2 Ohno-Higashi, Osakasayama, Osaka, 589-8511, Japan.
Hiroshi KajiDepartment of Physiology and Regenerative Medicine, Faculty of Medicine, Kindai University, 377-2 Ohno-Higashi, Osakasayama, Osaka, 589-8511, Japan. hkaji@med.kindai.ac.jp.ORCID http://orcid.org/0000-0001-7433-5135

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionGlucocorticoids delay fracture healing and induce osteoporosis. Angiogenesis plays an important role in bone repair after bone injury. Plasminogen activator inhibitor-1 (PAI-1) is the principal inhibitor of plasminogen activators and an adipocytokine that regulates metabolism. However, the mechanisms by which glucocorticoids delay bone repair remain unclear. MATERIALS AND

methodsTherefore, we herein investigated the roles of PAI-1 and angiogenesis in glucocorticoid-induced delays in bone repair after femoral bone injury using PAI-1-deficient female mice intraperitoneally administered dexamethasone (Dex).

resultsPAI-1 deficiency significantly attenuated Dex-induced decreases in the number of CD31-positive vessels at damaged sites 4 days after femoral bone injury in mice. PAI-1 deficiency also significantly ameliorated Dex-induced decreases in the number of CD31- and endomucin-positive type H vessels and CD31-positive- and endomucin-negative vessels at damaged sites 4 days after femoral bone injury. Moreover, PAI-1 deficiency significantly mitigated Dex-induced decreases in the expression of vascular endothelial growth factor as well as hypoxia inducible factor-1α, transforming growth factor-β1, and bone morphogenetic protein-2 at damaged sites 4 days after femoral bone injury.

conclusionThe present results demonstrate that Dex-reduced angiogenesis at damaged sites during the early bone-repair phase after femoral bone injury partly through PAI-1 in mice.

Indexed as

DexamethasoneGlucocorticoidsNeovascularization, PhysiologicPlasminogen Activator Inhibitor 1AngiogenesisAnimalsBone Morphogenetic Protein 2FemaleFemurFracture HealingHypoxia-Inducible Factor 1, alpha SubunitMiceMice, Inbred C57BLMice, KnockoutPlatelet Endothelial Cell Adhesion Molecule-1Vascular Endothelial Growth Factor ABone Morphogenetic Protein 2DexamethasoneGlucocorticoidsHypoxia-Inducible Factor 1, alpha SubunitPlasminogen Activator Inhibitor 1Platelet Endothelial Cell Adhesion Molecule-1Vascular Endothelial Growth Factor AAngiogenesisBone repairGlucocorticoidPlasminogen activator inhibitor-1

Identifiers

PMID38704516

What OpenQuestion holds

Textmetadata
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.