MicroRNA-148a-3p is a candidate mediator of increased bone marrow adiposity and bone loss following spinal cord injury.


Journal

Frontiers in endocrinology
ISSN: 1664-2392
Titre abrégé: Front Endocrinol (Lausanne)
Pays: Switzerland
ID NLM: 101555782

Informations de publication

Date de publication:
2022
Historique:
received: 01 04 2022
accepted: 08 07 2022
entrez: 22 8 2022
pubmed: 23 8 2022
medline: 24 8 2022
Statut: epublish

Résumé

Spinal cord injury is often followed by osteoporosis characterized by rapid and severe bone loss. This leads to an increased risk of osteoporotic fracture in people with spinal cord injury, resulting in increased healthcare costs, morbidity, and mortality. Though it is common, the mechanisms underlying this osteoporosis are not completely understood and treatment options are limited. No biomarkers have been identified for predicting fracture risk. In this study, we sought to investigate microRNA mediated mechanisms relating to osteoporosis following spinal cord injury. We studied subjects with acute SCI (n=12), chronic SCI (n=18), and controls with no SCI (n=23). Plasma samples from all subjects underwent transcriptomic analysis to quantify microRNA expression, after which miR-148a-3p was selected for further study. We performed CT scans of the knee on all subjects with SCI and analyzed these scans to quantify bone marrow adipose tissue volume. MiR-148a-3p was upregulated in subjects with acute SCI vs chronic SCI, as well as in acute SCI vs no SCI. Subjects with chronic SCI had greater levels of marrow adiposity in the distal femoral diaphysis compared to subjects with acute SCI. MiR-148a-3p levels were negatively associated with distal femoral diaphysis marrow adiposity. A multivariable model showed that miR-148a-3p and BMI explained 24% of variation in marrow adiposity. A literature search revealed that miR-148a-3p has multiple bone and fat metabolism related targets. Our findings suggest that miR-148a-3p is a mediator of osteoporosis following spinal cord injury and a potential future therapeutic target.

Identifiants

pubmed: 35992108
doi: 10.3389/fendo.2022.910934
pmc: PMC9388741
doi:

Substances chimiques

MicroRNAs 0

Types de publication

Journal Article Research Support, U.S. Gov't, Non-P.H.S. Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

910934

Subventions

Organisme : NIAMS NIH HHS
ID : R01 AR064793
Pays : United States

Informations de copyright

Copyright © 2022 Lincoln, Morse, Troy, Mattson, Nguyen and Battaglino.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Samantha Lincoln (S)

Drexel University College of Medicine, Philadelphia, PA, United States.

Leslie R Morse (LR)

Department of Rehabilitation Medicine, University of Minnesota School of Medicine, Minneapolis, MN, United States.

Karen Troy (K)

Department of Biomedical Engineering, Worcester Polytechnic Institute, Worcester, MA, United States.

Nicole Mattson (N)

Department of Biomedical Engineering, Worcester Polytechnic Institute, Worcester, MA, United States.

Nguyen Nguyen (N)

Department of Rehabilitation Medicine, University of Minnesota School of Medicine, Minneapolis, MN, United States.

Ricardo A Battaglino (RA)

Department of Rehabilitation Medicine, University of Minnesota School of Medicine, Minneapolis, MN, United States.

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Classifications MeSH