Expression of nerve growth factor in the callus during fracture healing in a fracture model in aged mice.


Journal

Bio-medical materials and engineering
ISSN: 1878-3619
Titre abrégé: Biomed Mater Eng
Pays: Netherlands
ID NLM: 9104021

Informations de publication

Date de publication:
2022
Historique:
pubmed: 7 9 2021
medline: 16 3 2022
entrez: 6 9 2021
Statut: ppublish

Résumé

Impaired fracture healing results in extensive and prolonged disability and long-term pain. Previous studies reported that nerve growth factor (NGF) was expressed during fracture healing and that anti-NGF antibody improves physical activity associate with facture pain. However, NGF expression levels in delayed or non-union are not fully understood. We compared chronological changes in NGF in the callus of young mice after femur fracture with those in aged mice after femur fracture as a model of bone fracture in the elderly. We used young (age 8 weeks) and aged (age 10 months) male C57BL/6J mice. A fracture was generated in the femur. At 5, 7, 10, 14, 17, and 21 days after creation of a fracture, mRNA expression levels of Col2a1, Col10a1, NGF were evaluated using quantitative PCR. We examined NGF protein expression levels and localization in the callus at day 14 using ELISA and immunohistochemistry, respectively. Expression of NGF in the callus after femur fracture in aged mice was significantly greater than that in young mice at days 5, 7, 10, 17, and 21 days. NGF protein levels in the callus of aged mice were also significantly higher than that in young mice. Immunohistochemical staining showed that NGF was heavily expressed in hypertrophic chondrocytes in the callus in aged mice. It is suggested that delayed Col2a1 and Col10a1 expression reflects delayed chondrocyte formation and delayed chondrocyte maturation in aged mice and that higher NGF expression in aged mice at day 14 may be associated with the presence of remaining hypertrophic chondrocytes in callus with delaying endochondral ossification.

Sections du résumé

BACKGROUND BACKGROUND
Impaired fracture healing results in extensive and prolonged disability and long-term pain. Previous studies reported that nerve growth factor (NGF) was expressed during fracture healing and that anti-NGF antibody improves physical activity associate with facture pain. However, NGF expression levels in delayed or non-union are not fully understood.
OBJECTIVE OBJECTIVE
We compared chronological changes in NGF in the callus of young mice after femur fracture with those in aged mice after femur fracture as a model of bone fracture in the elderly.
METHODS METHODS
We used young (age 8 weeks) and aged (age 10 months) male C57BL/6J mice. A fracture was generated in the femur. At 5, 7, 10, 14, 17, and 21 days after creation of a fracture, mRNA expression levels of Col2a1, Col10a1, NGF were evaluated using quantitative PCR. We examined NGF protein expression levels and localization in the callus at day 14 using ELISA and immunohistochemistry, respectively.
RESULTS RESULTS
Expression of NGF in the callus after femur fracture in aged mice was significantly greater than that in young mice at days 5, 7, 10, 17, and 21 days. NGF protein levels in the callus of aged mice were also significantly higher than that in young mice. Immunohistochemical staining showed that NGF was heavily expressed in hypertrophic chondrocytes in the callus in aged mice.
CONCLUSIONS CONCLUSIONS
It is suggested that delayed Col2a1 and Col10a1 expression reflects delayed chondrocyte formation and delayed chondrocyte maturation in aged mice and that higher NGF expression in aged mice at day 14 may be associated with the presence of remaining hypertrophic chondrocytes in callus with delaying endochondral ossification.

Identifiants

pubmed: 34487017
pii: BME211284
doi: 10.3233/BME-211284
doi:

Substances chimiques

Nerve Growth Factor 9061-61-4

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

131-137

Auteurs

Hiroyuki Sekiguchi (H)

Department of Orthopedic Surgery, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.
Shonan University of Medical Sciences Research Institute, Chigasaki, Kanagawa, Japan.

Gen Inoue (G)

Department of Orthopedic Surgery, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.

Shintaro Shoji (S)

Department of Orthopedic Surgery, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.

Ryo Tazawa (R)

Department of Orthopedic Surgery, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.

Akiyoshi Kuroda (A)

Department of Orthopedic Surgery, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.

Masayuki Miyagi (M)

Department of Orthopedic Surgery, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.

Masashi Takaso (M)

Department of Orthopedic Surgery, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.

Kentaro Uchida (K)

Department of Orthopedic Surgery, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.
Shonan University of Medical Sciences Research Institute, Chigasaki, Kanagawa, Japan.

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Classifications MeSH