Related Experiment Videos
Excessive microvascular adaptation to changes in blood flow in mice lacking gene encoding for desmin
Laurent Loufrani1, Zhenlin Li, Bernard I Lévy
1Institut National de la Santé et de la Recherche Médicale U 541, IFR Circulation-Paris-Nord, Paris, France.
Arteriosclerosis, Thrombosis, and Vascular Biology
|October 16, 2002
Summary
Mice lacking desmin show impaired microvascular adaptation to altered blood flow, impacting mesenteric artery remodeling. This desmin deficiency may contribute to desmin-related myopathies.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Muscle Biology
Background:
- Desmin is a crucial intermediate filament protein for myocyte integrity.
- Absence of desmin leads to cardiomyopathies and microvascular dysfunction.
- Desmin deficiency results in smooth muscle hyporeactivity.
Purpose of the Study:
- To investigate the impact of desmin absence on mesenteric artery adaptation to altered blood flow.
- To compare desmin-deficient (Des-/-) mice with wild-type (Des+/+) mice.
Main Methods:
- Selective ligation of second-order mesenteric arteries to create low (LF) and high (HF) flow conditions.
- Measurement of arterial diameter using an arteriograph under controlled pressure and flow.
- Assessment of flow-dependent dilation and endothelial nitric oxide synthase (eNOS) expression.
Main Results:
- Desmin-deficient mice exhibited altered pressure-diameter relationships in both LF and HF arteries.
- Flow-dependent dilation was significantly reduced in Des-/- mice compared to Des+/+ mice.
- Endothelial NO synthase expression increased in HF arteries in both groups.
Conclusions:
- Desmin plays a critical role in microvascular remodeling in response to changes in blood flow.
- Desmin deficiency impairs the adaptive capacity of mesenteric arteries.
- These vascular dysfunctions may be implicated in desmin-related myopathies.