Research Paper Volume 12, Issue 9 pp 8652—8668
Plasma proteomic profiling of young and old mice reveals cadherin-13 prevents age-related bone loss
- 1 Aging Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea
- 2 Center for Theragnosis, Korea Institute of Science and Technology, Seoul, Republic of Korea
- 3 The Research Center for Cellular Homeostasis, Department of Life Science, Ewha Womans University, Seoul, Republic of Korea
- 4 Korea Basic Science Institute, Gwangju Center at Chonnam National University, Gwangju, Republic of Korea
- 5 Department of Functional Genomics, KRIBB School of Bioscience, Korea University of Science and Technology (UST), Daejeon, Republic of Korea
- 6 Department of Life Science and Research Institute for Natural Sciences, Hanyang University, Seoul, Republic of Korea
- 7 Department of Medicinal Biotechnology, College of Health Sciences, Dong-A University, Busan, Republic of Korea
- 8 KHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul, Republic of Korea
- 9 Division of Bio-Medical Science and Technology, KIST School, Korea University of Science and Technology, Seoul, Republic of Korea
- 10 Present address: Incepta Vaccine Limited, Dhamrai, Bangladesh
received: November 2, 2019 ; accepted: March 2, 2020 ; published: May 12, 2020 ;https://doi.org/10.18632/aging.103184
How to Cite
Copyright © 2020 Yang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The blood exhibits a dynamic flux of proteins that are secreted by the tissues and cells of the body. To identify novel aging-related circulating proteins, we compared the plasma proteomic profiles of young and old mice using tandem mass spectrometry. The expression of 134 proteins differed between young and old mice. We selected seven proteins that were expressed at higher levels in young mice, and confirmed their plasma expression in immunoassays. The plasma levels of anthrax toxin receptor 2 (ANTXR2), cadherin-13 (CDH-13), scavenger receptor cysteine-rich type 1 protein M130 (CD163), cartilage oligomeric matrix protein (COMP), Dickkopf-related protein 3 (DKK3), periostin, and secretogranin-1 were all confirmed to decrease with age. We then investigated whether any of the secreted proteins influenced bone metabolism and found that CDH-13 inhibited osteoclast differentiation. CDH 13 treatment suppressed the receptor activator of NF-κB ligand (RANKL) signaling pathway in bone marrow-derived macrophages, and intraperitoneal administration of CDH-13 delayed age-related bone loss in the femurs of aged mice. These findings suggest that low plasma CDH-13 expression in aged mice promotes aging-associated osteopenia by facilitating excessive osteoclast formation. Thus, CDH-13 could have therapeutic potential as a protein drug for the prevention of osteopenia.