AI Article Synopsis
- - Type H vessels play a crucial role in connecting blood vessel formation (angiogenesis) with bone growth (osteogenesis), influenced by signals from sympathetic nerves, particularly in the metaphysis area of bones.
- - When sympathetic activity is stimulated (like through isoproterenol injection), there's a decrease in type H vessels and overall bone mass, while a lack of beta-2-adrenergic receptors helps maintain both vessel and bone mass under normal conditions.
- - The study indicates that sympathetic nerves indirectly affect blood vessel formation by interacting with mesenchymal stem cells, which modify gene expressions in endothelial cells, and suggests that targeting beta-adrenergic activity with drugs like propranolol could help protect bone health during estrogen deficiency.
Article Abstract
Type H vessels couple angiogenesis with osteogenesis, while sympathetic cues regulate vascular and skeletal function. The crosstalk between sympathetic nerves and type H vessels in bone remains unclear. Here, we first identify close spatial connections between sympathetic nerves and type H vessels in bone, particularly in metaphysis. Sympathoexcitation, mimicked by isoproterenol (ISO) injection, reduces type H vessels and bone mass. Conversely, beta-2-adrenergic receptor (ADRB2) deficiency maintains type H vessels and bone mass in the physiological condition. experiments reveal indirect sympathetic modulation of angiogenesis via paracrine effects of mesenchymal stem cells (MSCs), which alter the transcription of multiple angiogenic genes in endothelial cells (ECs). Furthermore, Notch signaling in ECs underlies sympathoexcitation-regulated type H vessel formation, impacting osteogenesis and bone mass. Finally, propranolol (PRO) inhibits beta-adrenergic activity and protects type H vessels and bone mass against estrogen deficiency. These findings unravel the specialized neurovascular coupling in bone homeostasis and regeneration.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10481296 | PMC |
| http://dx.doi.org/10.1016/j.isci.2023.107455 | DOI Listing |
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