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Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model

Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model

Published on: September 3, 2020

Cardiac pressure overload initiates a systemic stem cell response.

Amanda Finan¹, Matthew Kiedrowski, Benjamin A Turturice

¹Department of Molecular Biology and Microbiology, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA.

|May 26, 2012

Summary

Cardiac pressure overload triggers a systemic stem cell response. Endothelial progenitor cells (EPCs) and SSEA-1(+) cells mobilize to the heart, indicating a coordinated repair mechanism.

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Assessing Stem Cell DNA Integrity for Cardiac Cell Therapy

Assessing Stem Cell DNA Integrity for Cardiac Cell Therapy

Published on: January 25, 2019

Area of Science:

Cardiovascular Biology
Stem Cell Biology
Regenerative Medicine

Background:

Acute cardiac injury activates resident and non-cardiac stem cells.
Cardiac pressure overload (PO) is a significant stressor impacting cardiac repair mechanisms.

Purpose of the Study:

To define the pattern of peripheral stem cell and cardiac stem cell (CSC) activation following acute cardiac pressure overload.
To investigate the systemic and local stem cell responses to transaortic constriction (TAC).

Main Methods:

Pressure overload was induced in mice via transaortic constriction (TAC).
Cardiac stem cells (CSCs), endothelial progenitor cells (EPCs), hematopoietic stem cells (HSCs), and stage-specific embryonic antigen (SSEA)-1(+) cells were analyzed in the heart, spleen, and bone marrow using flow cytometry.

Main Results:

A systemic stem cell response involving EPCs and SSEA-1(+) cells was observed, with increased levels in the heart post-TAC.
Local SSEA-1(+) cell proliferation in the heart preceded increased myocardial stem cell numbers; however, EPC and CSC proliferation in the heart was not significant.
Systemic response included biphasic loss of splenic SSEA-1(+) cells and decreased bone marrow/spleen EPCs, with proliferation occurring after local depletion.

Conclusions:

An orchestrated systemic stem cell response, particularly involving EPCs and SSEA-1(+) cells, occurs in response to TAC.
Increased SSEA-1(+) cells and EPCs in the heart post-pressure overload likely result from both local proliferation and systemic recruitment.