Unexpected discovery of cardiac lymphatic vessels

In the study, published in the journal Circulation Research, researchers at the University of North Carolina School of Medicine identified a protein called VE-cadherin that is a key factor in maintaining the lymphatic vessels that serve the heart

"Everyone assumed that the lymphatic vessels of the heart would be critical for preventing abnormal accumulation of fluid after cardiac injury, but our study suggests that may not be the case," said study senior author Kathleen Caron, Ph.

The scientists used a group of mice engineered so that the VE-cadherin gene could be selectively deleted from lymphocytes at specific times

In experiments led by UNC-Chapel Hill graduate students Natalie Harris and Natalie Nielsen, the researchers found that deletion of the VE-cadherin gene caused severe degeneration of the heart's lymphatic vessels in newborn mice, and even in adult mice

But the researchers also used these cardiolymph-deficient mice as a new model to study the role of cardiolymph in normal heart function and heart repair after injury

The hearts of mice with few lymphatic vessels appeared to beat and pump normally, compared with those of mice with normal cardiac lymphatic vessels

Scientists studying the heart generally agree that cardiac lymphatic vessels play an important role in supporting normal heart function, but also in repair after injury

"This intriguing mouse model tells us that preventing cardiac edema may not be the primary function of the heart's lymphatic vessels after injury," said Caron, who is also a member of the McAllister Heart Institute at UNC

Based on their new findings, Caron and colleagues plan to explore whether lymphatic vessels have other important functions in supporting the heart

This research was supported by grants from the National Institutes of Health (nih) (HL1290986, DK119145, T32HL069768, F31 HL143836, T32CA071341, T32GM133364-01A1, R35HL155656, RO1 HL142905) and the American Heart Association

Journal Reference :

1. Brandon J.