Key result
Desmin deficiency in mice resulted in lower carotid artery distensibility, increased wall viscosity, and significantly lower rupture pressure (1500+/-200 mmHg vs 2100+/-80 mmHg in wild-type).
Desmin is essential to maintain proper viscoelastic properties, structure, and mechanical strength of the vascular wall in a mouse model.
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Desmin deficiency impairs arterial mechanics in mice; hypothesis-generating for vascular disease mechanisms and should not change practice.
OBJECTIVE: Our aim was to determine in desmin homozygous mutant mice the viscoelastic properties, the mechanical strength and the structure of the carotid artery. METHODS: To assess the viscoelastic properties of large arteries, we have performed an in vivo analysis of the diameter-, and distensibility-pressure curves of the common carotid artery (CCA) in homozygous (Des -/-), heterozygous (Des +/-) and wild-type (Des +/+) mice. To evaluate the mechanical strength, we have measured the in vitro intraluminal pressure producing the rupture of the carotid artery wall. The structure analysis of the arterial wall was based on histology and electronic microscopy. RESULTS: A lower distensibility and an increase of arterial wall viscosity were observed in Des -/- compared with Des +/+. Arterial thickness of Des -/- was similar to those of Des +/+, without changes in elastin and collagen contents. Electron microscopy revealed that the perimeter of cellular fingerlike-projections was smaller in Des -/-, indicating that the cells have lost part of their connections to the extracellular matrix. The rupture pressure was significantly lower in Des -/- (1500+/-200 mmHg) compared with Des +/+ (2100+/-80 mmHg) indicating a lower mechanical strength of the vascular wall. No significant difference was found between Des +/- and Des +/+. CONCLUSION: The desmin is essential to maintain proper viscoelastic properties, structure and mechanical strength of the vascular wall.
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Lacolley et al. (2001) studied Desmin deficiency. Desmin deficiency (Des -/-) vs. Wild-type (Des +/+) and heterozygous (Des +/-) mice was evaluated on Rupture pressure of the carotid artery wall. Desmin deficiency in mice resulted in lower carotid artery distensibility, increased wall viscosity, and significantly lower rupture pressure (1500+/-200 mmHg vs 2100+/-80 mmHg in wild-type).
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