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Plasma proteomic profiling of young and old mice reveals cadherin-13 prevents age-related bone loss
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...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244053/ https://www.ncbi.nlm.nih.gov/pubmed/32396872 http://dx.doi.org/10.18632/aging.103184 |
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author | Yang, Yong Ryoul Kabir, Mohammad Humayun Park, Jin Hee Park, Jae-Il Kang, Jae Sook Ju, Shinyeong Shin, Yeo Jin Lee, Seung Min Lee, Jaemin Kim, Seokho Lee, Kwang-Pyo Lee, Soo Young Lee, Cheolju Kwon, Ki-Sun |
author_facet | Yang, Yong Ryoul Kabir, Mohammad Humayun Park, Jin Hee Park, Jae-Il Kang, Jae Sook Ju, Shinyeong Shin, Yeo Jin Lee, Seung Min Lee, Jaemin Kim, Seokho Lee, Kwang-Pyo Lee, Soo Young Lee, Cheolju Kwon, Ki-Sun |
author_sort | Yang, Yong Ryoul |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7244053 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Impact Journals |
record_format | MEDLINE/PubMed |
spelling | pubmed-72440532020-06-03 Plasma proteomic profiling of young and old mice reveals cadherin-13 prevents age-related bone loss Yang, Yong Ryoul Kabir, Mohammad Humayun Park, Jin Hee Park, Jae-Il Kang, Jae Sook Ju, Shinyeong Shin, Yeo Jin Lee, Seung Min Lee, Jaemin Kim, Seokho Lee, Kwang-Pyo Lee, Soo Young Lee, Cheolju Kwon, Ki-Sun Aging (Albany NY) Research Paper 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. Impact Journals 2020-05-12 /pmc/articles/PMC7244053/ /pubmed/32396872 http://dx.doi.org/10.18632/aging.103184 Text en Copyright © 2020 Yang et al. http://creativecommons.org/licenses/by/3.0/ 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. |
spellingShingle | Research Paper Yang, Yong Ryoul Kabir, Mohammad Humayun Park, Jin Hee Park, Jae-Il Kang, Jae Sook Ju, Shinyeong Shin, Yeo Jin Lee, Seung Min Lee, Jaemin Kim, Seokho Lee, Kwang-Pyo Lee, Soo Young Lee, Cheolju Kwon, Ki-Sun Plasma proteomic profiling of young and old mice reveals cadherin-13 prevents age-related bone loss |
title | Plasma proteomic profiling of young and old mice reveals cadherin-13 prevents age-related bone loss |
title_full | Plasma proteomic profiling of young and old mice reveals cadherin-13 prevents age-related bone loss |
title_fullStr | Plasma proteomic profiling of young and old mice reveals cadherin-13 prevents age-related bone loss |
title_full_unstemmed | Plasma proteomic profiling of young and old mice reveals cadherin-13 prevents age-related bone loss |
title_short | Plasma proteomic profiling of young and old mice reveals cadherin-13 prevents age-related bone loss |
title_sort | plasma proteomic profiling of young and old mice reveals cadherin-13 prevents age-related bone loss |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244053/ https://www.ncbi.nlm.nih.gov/pubmed/32396872 http://dx.doi.org/10.18632/aging.103184 |
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