Desloratadine inhibits heterotopic ossification by suppression of BMP2-Smad1/5/8 signaling.


Journal

Journal of orthopaedic research : official publication of the Orthopaedic Research Society
ISSN: 1554-527X
Titre abrégé: J Orthop Res
Pays: United States
ID NLM: 8404726

Informations de publication

Date de publication:
06 2021
Historique:
received: 20 05 2019
accepted: 30 01 2020
pubmed: 12 2 2020
medline: 3 9 2021
entrez: 12 2 2020
Statut: ppublish

Résumé

Heterotopic ossification (HO) is a pathological condition in which ectopic bone forms within soft tissues such as skeletal muscle. Human platelet-derived growth factor receptor α positive (PDGFRα+) cells, which were proved to be the original cells of HO were incubated in osteogenic differentiation medium with Food and Drug Administration-approved compounds. Alkaline phosphatase activity was measured as a screening to inhibit osteogenic differentiation. For the compounds which inhibited osteogenic differentiation of PDGFRα+ cells, we examined dose dependency of its effect using alizarin red S staining and its cell toxicity using WST-8. In addition, regulation of bone morphogenetic proteins (BMP)-Smad signaling which is the major signal of osteogenic differentiation was investigated by Western blotting to elucidate the mechanism of osteogenesis inhibitory effect by the compound. In vivo experiment, complete transverse incision of Achilles tendons in mice was made and mice were fed the compound by mixing with drinking water after operation. Ten weeks after operation, we assessed and quantified HO by micro-computed tomography scan. Intriguingly, we discovered desloratadine inhibited osteogenic differentiation of PDGFRα+ cells using the drug repositioning method. Desloratadine inhibited osteogenic differentiation of the cells dose dependently without cell toxicity. Desloratadine suppressed phosphorylation of Smad1/5/8 induced by BMP2 in PDGFRα+ cells. In Achilles tenotomy mice model, desloratadine treatment significantly inhibited ectopic bone formation compared with control. In conclusion, we discovered desloratadine inhibited osteogenic differentiation using human PDGFRα+ cells and proved its efficacy using Achilles tenotomy ectopic bone formation model in vivo. Our study paved the way to inhibit HO in early clinical use because of its guaranteed safety.

Identifiants

pubmed: 32043642
doi: 10.1002/jor.24625
doi:

Substances chimiques

Bone Morphogenetic Protein 2 0
Smad Proteins 0
Loratadine 7AJO3BO7QN
Receptor, Platelet-Derived Growth Factor alpha EC 2.7.10.1
desloratadine FVF865388R

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1297-1304

Informations de copyright

© 2020 Orthopaedic Research Society. Published by Wiley Periodicals, Inc.

Références

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Auteurs

Taiki Kusano (T)

Department of Orthopaedic Surgery, Graduate School of Medicine, Nagoya University, Nagoya, Japan.
Division for Therapies against Intractable Diseases, Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Japan.
Division of Neurological Diseases and Cancer, Graduate School of Medicine, Nagoya University, Nagoya, Japan.

Masashi Nakatani (M)

Division for Therapies against Intractable Diseases, Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Japan.

Naoki Ishiguro (N)

Department of Orthopaedic Surgery, Graduate School of Medicine, Nagoya University, Nagoya, Japan.

Kinji Ohno (K)

Division of Neurological Diseases and Cancer, Graduate School of Medicine, Nagoya University, Nagoya, Japan.

Naoki Yamamoto (N)

Center for Joint Research Facilities Support, Fujita Health University, Research Promotion and Support Headquarters, Toyoake, Japan.

Mitsuhiro Morita (M)

Department of Orthopaedic Surgery, Fujita Health University, Toyoake, Japan.

Harumoto Yamada (H)

Department of Orthopaedic Surgery, Fujita Health University, Toyoake, Japan.

Akiyoshi Uezumi (A)

Department of Geriatric Medicine, Tokyo Metropolitan Institute of Gerontology, Itabashi, Tokyo, Japan.

Kunihiro Tsuchida (K)

Division for Therapies against Intractable Diseases, Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Japan.

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