Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Selective microvascular dysfunction in mice lacking the gene encoding for desmin.

Laurent Loufrani1, Khalid Matrougui, Zhenlin Li

  • 1Institut National de la Santé et de la Recherche Médicale (INSERM) U 541, IFR-Circulation-Paris-Nord, Paris VII University, Paris, France.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|December 1, 2001
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

STIM1-dependent treg dysfunction promotes cardiometabolic HFpEF: insights from patients and animal studies.

Cardiovascular diabetology·2026
Same author

Proteomic Profiling of Endothelial Cells Under Laminar Shear Stress Confirms the Importance of KLF4 in the Regulation of Membrane Protein Expression Compared to Oscillatory Flow.

Journal of proteome research·2026
Same author

Aortic Segments-Depending Hypertensive Remodeling Is Driven by Mitochondrial Fusion Dysfunction.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology·2026
Same author

Deletion of STIM1 in Treg cells protects against lung fibrosis and associated cardiovascular complications in a pre-clinical mouse model.

Redox biology·2026
Same author

Characteristics of sudden cardiac arrest during endurance racing: a decade of the Paris registry.

Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology·2026
Same author

Integrin α<sub>v</sub> contributes to the regulation of vascular smooth muscle cell stiffness.

Scientific reports·2026

Desmin is crucial for vascular smooth muscle cells, particularly in small arteries. Its absence impairs vascular tone and dilation, potentially contributing to desmin-related myopathies.

Area of Science:

  • Vascular biology and smooth muscle cell function.
  • Intermediate filament protein research.
  • Cardiovascular disease mechanisms.

Background:

  • Desmin is vital for muscle cell integrity and contractility, with its absence linked to cardiomyopathies.
  • Desmin distribution in arteries is heterogeneous, suggesting potential roles in vascular disorders.
  • The specific function of desmin in vascular smooth muscle cells and overall vascular health remains largely unexplored.

Purpose of the Study:

  • To investigate the role of desmin in vascular endothelial and muscular functions.
  • To compare vascular contractile and dilatory responses in arteries from desmin-deficient mice versus controls.
  • To elucidate the contribution of desmin to vascular tone regulation and blood flow supply.

Main Methods:

Related Experiment Videos

  • Utilized arteriography to study carotid and mesenteric resistance arteries from desmin-deficient (des-/-) and control (des+/+) mice.
  • Assessed pressure-induced myogenic tone, agonist-induced tone, and flow/acetylcholine-induced dilations.
  • Examined desmin localization within arterial tissues, confirming its presence exclusively in smooth muscle cells.

Main Results:

  • Desmin was found exclusively in vascular smooth muscle cells.
  • While myogenic tone was unaffected, agonist-induced tone was reduced in resistance arteries of des-/- mice.
  • Both endothelium-dependent and independent dilations were significantly decreased in resistance arteries lacking desmin.
  • Large arteries showed normal vascular reactivity, contrasting with significant deficits in small resistance arteries.

Conclusions:

  • Desmin is essential for vascular smooth muscle cells, particularly within resistance arteries.
  • The absence of desmin impairs vascular tone control and dilation, impacting optimal blood flow.
  • This microvascular dysfunction in desmin deficiency may be a key factor in desmin-related myopathies.