| Autor: |
Halloran D; Department of Biological Sciences, University of Delaware, Newark, DE 19716, USA., Pandit V; Department of Biological Sciences, University of Delaware, Newark, DE 19716, USA., Chukwuocha K; Department of Biological Sciences, University of Delaware, Newark, DE 19716, USA., Nohe A; Department of Biological Sciences, University of Delaware, Newark, DE 19716, USA. |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of developmental biology [J Dev Biol] 2024 Nov 18; Vol. 12 (4). Date of Electronic Publication: 2024 Nov 18. |
| DOI: |
10.3390/jdb12040030 |
| Abstrakt: |
During aging, disruptions in various signaling pathways become more common. Some older patients will exhibit irregular bone morphogenetic protein (BMP) signaling, which can lead to osteoporosis (OP)-a debilitating bone disease resulting from an imbalance between osteoblasts and osteoclasts. In 2002, the Food and Drug Administration (FDA) approved recombinant human BMP-2 (rhBMP-2) for use in spinal fusion surgeries as it is required for bone formation. However, complications with rhBMP-2 arose and primary osteoblasts from OP patients often fail to respond to BMP-2. Although patient samples are available for study, previous medical histories can impact results. Consequently, the C57BL/6 mouse line serves as a valuable model for studying OP and aging. We find that BMP receptor type Ia (BMPRIa) is upregulated in the bone marrow stromal cells (BMSCs) of 15-month-old mice, consistent with prior data. Furthermore, conjugating BMP-2 with Quantum Dots (QDot ® s) allows effective binding to BMPRIa, creating a fluorescent tag for BMP-2. Furthermore, after treating BMSCs with methyl-β-cyclodextrin (MβCD), a disruptor of cellular endocytosis, BMP signaling is restored in 15-month-old mice, as shown by von Kossa assays. MβCD has the potential to restore BMPRIa function, and the BMP signaling pathway offers a promising avenue for future OP therapies. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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