Myovascular Mechanisms of Cardiac Growth and Regeneration

NIH RePORTER · NIH · R01 · $539,063 · view on reporter.nih.gov ↗

Abstract

ABSTRACT: We, and others, have determined that cardiomyocyte (CM) proliferation is dependent on cardiac endothelial cells (CECs). Proliferating CECs are spatiotemporally coupled to proliferating CMs in the neonatal mouse heart; loss of CECs leads to decreased CM proliferation; and higher levels of the master angiogenic factor Vegfa promote cardiac growth in zebrafish, neonatal mice, and humans. Based on these studies, our overall hypothesis is that activated, proliferating CECs instruct CM proliferation. Here, we propose studies to determine how CECs promote CM proliferation. We will use scRNA-seq and spatial modeling to identify the specific subset of CECs physically associated with proliferating CMs; we will determine how Ezh2- mediated chromatin remodeling coordinates CEC activation with CM proliferation; and we will define the potency of CEC-induced growth factors to stimulate CM proliferation. This work will result in new cellular, epigenetic, and paracrine mechanisms for CEC-induced cardiac growth and has high potential to inform methods for therapeutic heart regeneration.

Key facts

NIH application ID
10364312
Project number
1R01HL157277-01A1
Recipient
DUKE UNIVERSITY
Principal Investigator
RAVI KARRA
Activity code
R01
Funding institute
NIH
Fiscal year
2022
Award amount
$539,063
Award type
1
Project period
2022-01-01 → 2026-12-31