Related Experiment Video
Updated: Aug 31, 2025
Assessing Therapeutic Angiogenesis in a Murine Model of Hindlimb Ischemia
Published on: June 8, 2019
Recovery of Ischemic Limb and Femoral Artery Endothelial Function Are Preserved in Mice with Dextran Sodium
Hao Wu1,2, Qiang Zhu1, Xuanyou Liu1
1Center for Precision Medicine and Division of Cardiovascular Medicine, University of Missouri School of Medicine, Columbia, MO 65212, USA.
Insights
Chronic colitis in female mice did not impair femoral artery endothelial function or limb ischemia recovery. This study found no significant impact on blood flow or vascular density in affected limbs.
Area of Science:
- Vascular Biology
- Inflammatory Bowel Disease Research
- Endothelial Function Studies
Background:
- Inflammatory bowel disease (IBD) is linked to systemic inflammation, endothelial dysfunction, and peripheral artery disease.
- Previous research indicated impaired abdominal aortic endothelial cell function in female mice with chronic colitis.
Purpose of the Study:
- To investigate if experimental colitis affects femoral artery endothelial function in female mice.
- To determine if colitis impairs recovery from limb ischemia in female mice.
Main Methods:
- A chronic colitis model was induced in female mice using dextran sodium sulfate (DSS).
- Unilateral hind limb ischemia was surgically created via femoral artery ligation.
- Evaluated limb blood perfusion, vascular density, reactive oxygen species (ROS) levels, and cytokine profiles.
- Assessed ex vivo femoral artery vasodilation using acetylcholine and nitroglycerin.
Main Results:
- DSS-induced colitis significantly elevated plasma levels of pro-inflammatory cytokines (TNF-α, IL-6, IL-17).
- No significant increase in ROS levels was observed in ischemic muscle tissue.
- Femoral artery endothelium-dependent and -independent vasodilation remained unchanged.
- Ischemic limb function, blood flow recovery, and capillary density were preserved.
Conclusions:
- Experimental chronic colitis in female mice did not significantly impact femoral artery endothelial function.
- Colitis did not impair the recovery of ischemic limb function or vascularity in this model.
Abstract:
Inflammatory bowel disease (IBD) produces significant systemic inflammation and increases the risk of endothelial dysfunction and peripheral artery disease. Our recent study demonstrated that abdominal aortic endothelial cell function was impaired selectively in female mice with chronic colitis. This study aimed to test the hypothesis that experimental colitis leads to femoral artery endothelial cell dysfunction and impairs limb ischemia recovery in female mice. An experimental chronic colitis model was created in female C57BL/6 mice with dextran sodium sulfate (DSS) treatment. Unilateral hind limb ischemia was produced by femoral artery ligation. Limb blood perfusion, vascular density, tissue ROS levels, and plasma levels of proinflammatory cytokines were assessed. Femoral artery endothelium-dependent and -independent vasodilation of the contralateral limb were evaluated ex vivo using acetylcholine and nitroglycerin, respectively. As expected, the plasma levels of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-α), interleukin (IL)-6, and IL-17, were significantly increased in the DSS-induced colitis model. However, ROS levels in the ischemic muscle tissues were not significantly increased in colitis model as compared to the controls. There were no significant changes in endothelium-dependent or -independent vasodilation of the femoral artery between colitis model and the control. Recovery of function and blood flow in the ischemic limb and capillary density in the ischemic gastrocnemius muscle were preserved in the colitis model as compared with the control. The data demonstrated that DSS-induced chronic colitis had no significant impact on femoral artery endothelial function or ischemic limb recovery in female mice.
