Related Experiment Video
Updated: Aug 1, 2026
04:30
A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
Bone re/modeling is more dynamic in the endothelial nitric oxide synthase(-/-) mouse
1Division of Endocrinology, Metabolism and Lipids, Emory University, Atlanta, Georgia 30332, USA.
Endocrinology
|June 10, 2006
Summary
Endothelial NO synthase (eNOS) mitigates bone loss after estrogen deprivation. Mice lacking eNOS show exaggerated bone remodeling, indicating eNOS
Area of Science:
- Endocrinology
- Bone Biology
- Molecular Signaling
Background:
- Nitric oxide (NO) is an estrogen-regulated molecule involved in bone maturation and remodeling.
- The role of bone-cell-secreted NO in ovariectomy-induced bone turnover requires further investigation.
Purpose of the Study:
- To investigate the expression of endothelial NO synthase (eNOS) in bone cells following estrogen deprivation.
- To determine the long-term effects of eNOS on ovariectomy-induced bone loss and remodeling.
Main Methods:
- Examined eNOS expression in bone and marrow stromal cells at intervals up to 10 weeks post-ovariectomy.
- Analyzed bone mineral density in wild-type and eNOS knockout mice for 10 weeks post-ovariectomy.
Main Results:
- Ovariectomy initially decreased bone cell eNOS production, followed by a significant rebound and sustained high levels.
- Ovariectomized eNOS knockout mice exhibited exaggerated bone remodeling compared to wild-type controls.
- eNOS knockout mice continued to accrue bone mass at a high rate, unlike estrogen-replete wild-type mice.
Conclusions:
- eNOS plays a crucial role in mitigating ovariectomy-induced bone remodeling.
- eNOS regulates the transition from basal bone modeling to bone remodeling.
