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CD34, CD45, and CD14. From immunological standpoint MSCs (widely described
as MHC I+, MHC II−, CD40−, CD80−, CD86−) are regarded as nonimmunogenic and,
therefore, transplantation into an allogeneic host may not require immunosuppres-
sion. MHC class I may activate T cells, but because of absence of costimulatory
molecules, a secondary signal would not engage, leaving the T cells anergic [ 9 ].
It has been shown that MSCs, when transplanted systemically, are able to migrate
to sites of injury suggesting that MSCs possess migratory capacity. These properties
of MSCs make them ideal candidates for tissue engineering [ 10 ]. The in vivo behav-
ior of MSCs is less well known as compared to the in vitro characterization of these
cells. Prior studies have either performed site directed or systemic administration of
cells. For example, repair of infarcted myocardium has been studied in multiple
studies using bone marrow cells [ 11 – 13 ]. Injury to a target organ is sensed by dis-
tant stem cells, which migrate to the site of damage and undergo alternate stem cell
differentiation [ 14 ]; these events promote structural and functional repair [ 15 ].
Animal models have conclusively shown that transplantation of BMCs induces
angiogenesis. BMCs differentiate into cardiac-like muscle cells in culture and
in vivo in ventricular scar tissue and improve myocardial function [ 16 ].
The mechanism by which MSCs home to tissues is not yet fully understood, but
it is likely that injured tissue expresses specific receptors or ligands to facilitate traf-
ficking, adhesion, and infiltration of MSCs to the site of injury. Given considerable
potential for myocardial repair using stem cells, it is pertinent to use appropriate
imaging techniques to monitor myocardial homing and biodistribution of these cells
after therapeutic application in patients.
8.2 Cardiovascular Applications of Stem Cells
Cardiovascular disease remains the number one cause of morbidity and mortality in
the United States and Europe. Over the past decade or so, several animal studies and
clinical trials have supported the use of stem cells as a potential therapeutic modal-
ity in patients with acute myocardial infarction and end-stage congestive heart fail-
ure. Several different types of cells have been used in both animal and human studies
to promote repair of the damaged myocardium. For cardiovascular applications,
adult and embryonic stem (ES) cells are the two main sources. These can be deliv-
ered either through transvascular route or direct injection into the left ventricular
wall. The goal is to deliver enough cells at the site of injury to maximize restoration
of cardiac function [ 17 , 20 ]. Injecting stem cells in the setting of myocardial infarc-
tion can promote cardiomyocyte formation with improvement in systolic function
[ 18 ]. Improvement in systolic function has also been shown in cardiomyopathies as
seen on cardiac MRI imaging following autologous bone marrow transplantation
suggesting homing of stem cells in the injured myocardium [ 19 – 21 ].
A study conducted at the authors’ institution used cardiac amyloidosis as a model
for infiltrative cardiac disease to study outcome of stem cell therapy [ 19 ]. In cases
of amyloidosis secondary to multiple myeloma, the underlying plasma cell dyscrasia
S. Raina et al.