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Related Experiment Video

Updated: Jun 27, 2026

Isolation of Endocardial and Coronary Endothelial Cells from the Ventricular Free Wall of the Rat Heart

Isolation of Endocardial and Coronary Endothelial Cells from the Ventricular Free Wall of the Rat Heart

Published on: April 15, 2020

Extracellular Vesicles Link Cerebral Ischemia to Coronary Microvascular Dysfunction - Role for RGD Motif-Activated

Marta Balogh¹, Melina Tangos^2,3,4, Vijay S Patel⁵

¹Department of Physiology, Medical College of Georgia, Augusta University, Augusta, GA, 30912, USA.

Journal of Cardiovascular Translational Research

|June 25, 2026

Summary

Ischemic stroke impairs heart blood vessel function through circulating factors. This study reveals extracellular vesicles mediate this brain-heart connection, offering potential therapeutic targets.

Keywords:

Arginine-Glycine-Aspartic Acid Endothelin Endothelium Ischemic Stroke Microparticle Myocardial Ischemia Vesicle

Related Experiment Videos

Last Updated: Jun 27, 2026

Isolation of Endocardial and Coronary Endothelial Cells from the Ventricular Free Wall of the Rat Heart

Isolation of Endocardial and Coronary Endothelial Cells from the Ventricular Free Wall of the Rat Heart

Published on: April 15, 2020

Area of Science:

Cardiovascular Research
Neurology
Vascular Biology

Background:

Ischemic stroke increases the risk of subsequent cardiac ischemic events.
Mechanisms linking cerebral ischemia to coronary dysfunction are not fully understood.
Circulating factors released after cerebral ischemia may directly impair coronary microvascular function.

Purpose of the Study:

To investigate whether ischemic stroke directly impairs coronary microvascular function.
To identify the role of circulating factors, specifically extracellular vesicles, in this process.
To elucidate the signaling pathways involved in stroke-induced coronary dysfunction.

Main Methods:

Assessed coronary arteriole (CA) vasodilator function in patients with prior ischemic stroke.
Utilized a rat model of transient middle cerebral artery occlusion (MCAO).
Isolated extracellular vesicles (EVs) from post-ischemic rats and delivered them into rat CA lumen.
Administered RGD peptide and endothelin ETA receptor antagonist (BQ-123) to rat CAs.

Main Results:

Coronary arteriole vasodilator function was reduced in patients with prior ischemic stroke.
MCAO in rats impaired CA vasodilator function.
EVs from ischemic rats impaired vasodilation when delivered into rat CAs.
RGD peptide attenuated flow-induced vasodilation, an effect blocked by BQ-123.

Conclusions:

Ischemic stroke directly induces coronary microvascular dysfunction.
Circulating extracellular vesicles play a key role in the brain-heart vascular axis.
RGD-motif-dependent activation of endothelin signaling mediates stroke-induced coronary dysfunction.
EV-mediated pathways represent potential therapeutic targets for post-stroke cardiac risk.