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ADAMTS5 deficiency in mice does not affect cardiac function.

Bianca Hemmeryckx¹, Paolo Carai¹, H Roger Lijnen¹

¹Department of Cardiovascular Sciences, Center for Molecular and Vascular Biology, KU Leuven, 3000 Leuven, Belgium.

Cell Biology International

|April 9, 2019

Summary

This summary is machine-generated.

ADAMTS5 deficiency impairs versican cleavage in the heart, particularly under high-fat diet conditions. However, this genetic alteration does not significantly impact overall cardiac function or electrophysiology in mice.

Keywords:

aggrecanase heart function obesity versican cleavage

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Area of Science:

Cardiovascular Biology
Extracellular Matrix Remodeling
Enzymology

Background:

The aggrecanase ADAMTS5 (A Disintegrin and Metalloproteinase with ThromboSpondin type 1 motifs, member 5) and its substrate versican are implicated in heart valve development.
ADAMTS5 deficiency has been shown to protect against diet-induced obesity, a cardiovascular disease risk factor.

Purpose of the Study:

To investigate the role of ADAMTS5 in cardiac function.
To assess the impact of ADAMTS5 deficiency on cardiac remodeling and electrophysiology under standard and high-fat diet conditions.

Main Methods:

Utilized ADAMTS5-deficient (Adamts5-/-) and wild-type (Adamts5+/+) mice fed standard or high-fat diets (HFD) for 15 weeks.
Analyzed cardiac function and electrophysiology via transthoracic echocardiogram and electrocardiogram.
Assessed versican cleavage by detecting the DPEEAE neo-epitope via Western blotting.

Main Results:

Versican cleavage was defective in the hearts of HFD-fed Adamts5-/- mice compared to wild-type controls.
ADAMTS5 deficiency led to increased diastolic posterior wall thickness and left ventricle volume in HFD-fed mice.
Ejection fraction, fractional shortening, stroke volume, and electrocardiogram parameters remained unaffected by ADAMTS5 deficiency or diet.

Conclusions:

ADAMTS5 deficiency impairs cardiac extracellular matrix versican cleavage.
Despite altered versican cleavage, cardiac function and electrophysiology are not markedly affected by ADAMTS5 deficiency, even under high-fat diet exposure.